Plasma corticosterone 1 hr post 4/g/kg EtOH [µg/dl]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD. 	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci 	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	01	65-115 days	65	115	Male	5-15	µg/dl	16.21	1.63	20.29	3.02	17.42	1.67	16.89	2.14	22.63	3.22	12.53	2.86	13.97	1.86	28.12	2.81			24.68	2.55	17.17	1.91	23.09	1.42	16.11	2.53	27.64	2.69	20.39	4.06					16.41	2.49	20.13	1.91			22.82	3.16	15.07	4.75	24.24	3.18	24.03	2.00	16.34	2.04																													12/26/2002			ETCORT4(1H)		ETCORT1	EtOH	4g/kg		JKB/AR	p. 1202, Fig 1	MRG 020402 with JKB by publication	8748968.01
Plasma corticosterone 1 hr post saline [µg/dl]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci 	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	03	65-115 days	65	115	Male	3-9	µg/dl	4.36	0.64	4.07	1.71	4.35	2.00	8.28	3.78	3.99	1.03	8.59	4.62	15.19	5.56	5.07	0.89			5.64	1.90	2.47	0.64	6.14	1.14	6.04	2.67	7.54	3.74	1.09	0.37					5.66	2.71	4.22	0.69			6.95	1.58	11.34	8.21	11.86	9.09	7.77	2.66	2.88	0.53																													12/26/2002			SALCORT (1H)		SALCORT1	Saline			JKB/AR	p. 1202, Fig 1	MRG 020402 with JKB by publication	8748968.03
Plasma corticosterone 6 hr post ETOH Male [µg/dl] [Plasma corticosterone 6 hours post 4/g/kg EtOH (Male), Unpublished means from same series of studies as reported in:  Roberts, Phillips, Belknap, Finn, Keith 1995, Behavioral Neurosci 109:1199-1208]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci 	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	99	65-115 days	65	115	Male		µg/dl							16.4		15.3		13.9		4.5				4.7		21.9		17.7		16.5		17.7		15.3		20						13.3		12.8		16.1		14.8		8.6		21.5		16.3		11.8		18.1		9.5		15.7																								12/27/2002			SALCORT(6H)		ETCORT6	EtOH	4g/kg		JKB/AR		MRG 020402 with JKB	8748968.99
Plasma corticosterone 6 hr post EtOH Female [µg/dl] [Plasma corticosterone 6 hours post 4/g/kg EtOH (Female)Unpublished means from same series of studies as reported in:  Roberts, Phillips, Belknap, Finn, Keith 1995, Behavioral Neurosci 109:1199-1208]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	98	65-115 days	65	115	Female		µg/dl	5		9		4		9		14		8		4		10		5		22		18		12		17		7		20		13				13		9		16		12		8		21		16		12		18		10		16																								12/27/2002			SALCORT(6HF)		ETCORT6F	EtOH	4g/kg		JKB/AR		MRG 020402 with JKB	8748968.98
Audiogenic seizure-mean severity score in response to pure tone [severity of seizure] 		The difference in susceptibility to audiogenic seizures (AGS) between C57BL/6J and DBA/2J inbred strains of mice is due to multiple genetic factors. AGS susceptibility was tested in 21-day-old mice from classical crosses, BXD recombinant inbred (RI) strains, a congenic DBA/2N.B6N-Ahb inbred strain and crosses between the BXD RI strains and DBA/2J. Analysis of these data reveals that the variation in AGS susceptibility between these two strains results from allelic differences at three or more loci. Most of the variation is due to allelic differences at two loci. The first, Asp-1 (formerly Ias), is a major gene located on chromosome 12, between Ah and D12 Nyul. The second, Asp-2 (formerly asp), is a minor gene located on chromosome 4, tightly linked to b. The negative correlation of brain stem Ca2(+)-ATPase activity and AGS susceptibility in the BXD RI strains suggests that the strain difference in Ca2(+)-ATPase activity is inherited as a polygenic trait and that Asp-1 and Asp-2 are linked to, or identical to, factors that influence Ca2(+)-ATPase activity.	Neumann PE, Seyfried TN.	Mapping of two genes that influence susceptibility to audiogenic seizures in crosses of C57BL/6J and DBA/2J mice	Behav Genet 	20(2)	307-323	Mar	1990		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2141254&dopt=Abstract	2141254		01	20-22 days	20	22	MF	10-63	Severity of seizure; 0=no response, 1=wild running, 2=clonic or tonic seizure 	0.07		1.88		0.2		1.92		1.64		0.14		0.57		1.85		1.04		0.3		0.1		0.33		1.94		0.21		0.07		0.73				1.92				1.16		1.09		0.36		1.29		1		0.09		0				1.89																								6/23/2003	MK Sullivan	MK Sullivan	AGS		AGS	 	60 sec exposure to pure tone 11KHx at 120db		JKB	p. 311, Table 1	MRG 120601 from publication	2141254.01
Morphine hypothermia DRC slope			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		01				Male			-4.58		-7.01		-7.06		-5.75		-6.33		-4.88		-7.36		-2.93				-2.02		-3.43		-3.75		-1.88		-1.31		-4.53						-2.73		-2.12		-5.29		-3.54		-6.06		-5.82		-7.5		-6.06																												-7.65		12/20/2002			MORTEMP		BDTEMP30	Morphine	Dose response across 8, 16, or 32 mg/kg i.p.		JKB	p. 319, Fig 3	MRG 011002; prior confirmation by JKB with data and publication	1632590.01
Morphine analgesia DRC slope			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		02				Male			26.8		59.7		50.1		63.4		30		30.5		62.7		27.6				33.9		25.8		31.2		25.5		36.7		39.1						15.2		10.9		44.3		59.8		35.4		46.3		34.7		24.3																												42.9		12/20/2002			MORHPL8		HOTPLATE	Morphine	Dose response across 8, 16, or 32 mg/kg i.p.		JKB	p. 319, Fig 3	MRG 011002; prior confirmation by JKB with data and publication	1632590.02
Straub tail Morphine DRC slope			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		03				Male			0.94		0.25		1.37		1.04		1.07		0.94		0.42		0.75				0.81		0.94		1.37		0.91		0.73		0.98						0.48		0.61		1.2		0.35		0.75		1.16		1.24		0.75																												0.78		12/20/2002			MORSTRAUB		STRAUB30	Morphine	Dose response across 8, 16, or 32 mg/kg i.p.		JKB	p. 319, Fig 3	MRG 011002; prior confirmation by JKB with data and publication	1632590.03
Saline body temp, degree C			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		04				Male		degrees celsius	37.5		37.7		38.1		37		37.2		38.3		37.4		37.3				38.4		37.8		37.6		36.6		37		38.4						36.8		37.3		37.5		37.5		37.9		38.5		37.8		38.8																												38.2		12/20/2002			SALTEMP		SAL_BTMP	Saline			JKB		MRG 011002; prior confirmation by JKB with data and publication	1632590.04
Saline hot plate latency, seconds			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		05				Male		seconds	20.2		21.3		22		19.5		11.8		8.8		31		18				14.1		11.6		12.8		13		11.9		20						13.8		16.1		12.2		13.5		15		15.5		22.9		9.8																												19.1		12/20/2002			SALHP8		SAL_HOTP	Saline			JKB		MRG 011002; prior confirmation by JKB with data and publication	1632590.05
Saline elevated open field activity, [Unpublished means from same series of studies as reported in:  Belknap & Crabbe, 1992 ANYAS 654:311-323]			Belknap JK, Crabbe JC.	Chromosome mapping of gene loci affecting morphine and amphetamine responses in BXD recombinant inbred mice	Ann NY Acad Sci	654	311-323	Jun 	1992 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1632590&dopt=Abstract	1632590		06				Male			15.44		6.39		9.34		12.15		9.24		15.25		8.4		8.675				14.49		6.43		11.84		7.315		10.25		12.72						7.95		8.3		5.925		6.945		8.26		8.58		5.25		12																														12/20/2002			SALACT(EOF)		SALACT	Saline			JKB		MRG 020402 with JKB	1632590.06
Baseline handling induced convulsions (HIC) 		Recombinant inbred (RI) mouse strains were developed primarily as a tool to detect and provisionally map major gene loci--those with effects large enough to cause a bimodal distribution in the trait of interest. This implied that progress toward gene mapping was possible only for gene loci accounting for at least half of the genetic variance. More recently, QTL (quantitative trait loci) approaches have been advanced that do not require bimodal distributions and are thus applicable to a much wider range of phenotypes. They offer the prospect of meaningful progress toward detecting and mapping minor as well as major gene loci affecting any trait of interest, provided there is a significant degree of genetic determination among the RI strains. This paper presents a review of RI gene mapping efforts concerning phenotypes related to drug abuse and presents new data for studies now in progress for nitrous oxide and acute ethanol withdrawal intensity. These two studies exemplify several strengths and limitations of the RI QTL approach.	Belknap JK, Metten P, Helms ML, O'Toole LA, Angeli-Gade S, Crabbe JC, Phillips TJ.	Quantitative trait loci (QTL) applications to substances of abuse: physical dependence studies with nitrous oxide and ethanol in BXD mice	Behav Genet 	23(2)	213-222	Mar	1993		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8512534&dopt=Abstract	8512534		01	100 days			Male			0.6995		0.3415		1.6835		2.0565		1.17045		0.3985		1.146		1.8895				0.6495		1.581		1.928		0.1625		0.4835		0.4165						0.7105		0.6315				0.091		0.125		1.5725		0.625		0.0985																														12/20/2002			BASEHIC		AVGAVB				JKB		MRG 011002; prior confirmation by JKB with data and publication	8512534.01
Nitrous oxide withdrawal handling induced convulsion (HIC) area under curve		Recombinant inbred (RI) mouse strains were developed primarily as a tool to detect and provisionally map major gene loci--those with effects large enough to cause a bimodal distribution in the trait of interest. This implied that progress toward gene mapping was possible only for gene loci accounting for at least half of the genetic variance. More recently, QTL (quantitative trait loci) approaches have been advanced that do not require bimodal distributions and are thus applicable to a much wider range of phenotypes. They offer the prospect of meaningful progress toward detecting and mapping minor as well as major gene loci affecting any trait of interest, provided there is a significant degree of genetic determination among the RI strains. This paper presents a review of RI gene mapping efforts concerning phenotypes related to drug abuse and presents new data for studies now in progress for nitrous oxide and acute ethanol withdrawal intensity. These two studies exemplify several strengths and limitations of the RI QTL approach.	Belknap JK, Metten P, Helms ML, O'Toole LA, Angeli-Gade S, Crabbe JC, Phillips TJ.	Quantitative trait loci (QTL) applications to substances of abuse: physical dependence studies with nitrous oxide and ethanol in BXD mice	Behav Genet	23(2)	213-222	Mar	1993 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8512534&dopt=Abstract	8512534		02	100 days			Male			5.68		13.24		6.85		1.17		15.6		4.57		5.35		20				2.2		10.15		2.55		1		1.33		3.8						8.87		3.36				6.5		6.67		9		6.94		5.62																														12/20/2002			N2OHIC(AUC)		NCOAUC	Nitrous Oxide	gas 75%	 	JKB		MRG 011002; prior confirmation by JKB with data and publication	8512534.02
Corrected peak for nitrous oxide withdrawal handling induced convulsions HIC		Recombinant inbred (RI) mouse strains were developed primarily as a tool to detect and provisionally map major gene loci--those with effects large enough to cause a bimodal distribution in the trait of interest. This implied that progress toward gene mapping was possible only for gene loci accounting for at least half of the genetic variance. More recently, QTL (quantitative trait loci) approaches have been advanced that do not require bimodal distributions and are thus applicable to a much wider range of phenotypes. They offer the prospect of meaningful progress toward detecting and mapping minor as well as major gene loci affecting any trait of interest, provided there is a significant degree of genetic determination among the RI strains. This paper presents a review of RI gene mapping efforts concerning phenotypes related to drug abuse and presents new data for studies now in progress for nitrous oxide and acute ethanol withdrawal intensity. These two studies exemplify several strengths and limitations of the RI QTL approach.	Belknap JK, Metten P, Helms ML, O'Toole LA, Angeli-Gade S, Crabbe JC, Phillips TJ.	Quantitative trait loci (QTL) applications to substances of abuse: physical dependence studies with nitrous oxide and ethanol in BXD mice	Behav Genet                                                                                     	23(2)	213-222	Mar	1993 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8512534&dopt=Abstract	8512534		03	100 days			Male			1.4	0.19	2.94	0.20	1.41	0.25	0.44	0.11	3.4	0.35	1.28	0.27	1.31	0.19	4.17	0.23			0.62	0.19	2.2	0.22	0.88	0.24	0.3	0.13	0.39	0.09	0.73	0.11					2.09	0.36	0.79	0.22			1.71	0.32	1.56	0.28	2	0.31	1.35	0.29	1.35	0.30																													12/20/2002			N2OHIC(PK)		NCORPK2	Nitrous Oxide	gas 75%		JKB		MRG 011002; prior confirmation by JKB with data and publication	8512534.03
Nitrous oxide withdrawal handling induced convulsions-difference from baseline (treated minus nontreated)		Recombinant inbred (RI) mouse strains were developed primarily as a tool to detect and provisionally map major gene loci--those with effects large enough to cause a bimodal distribution in the trait of interest. This implied that progress toward gene mapping was possible only for gene loci accounting for at least half of the genetic variance. More recently, QTL (quantitative trait loci) approaches have been advanced that do not require bimodal distributions and are thus applicable to a much wider range of phenotypes. They offer the prospect of meaningful progress toward detecting and mapping minor as well as major gene loci affecting any trait of interest, provided there is a significant degree of genetic determination among the RI strains. This paper presents a review of RI gene mapping efforts concerning phenotypes related to drug abuse and presents new data for studies now in progress for nitrous oxide and acute ethanol withdrawal intensity. These two studies exemplify several strengths and limitations of the RI QTL approach.	Belknap JK, Metten P, Helms ML, O'Toole LA, Angeli-Gade S, Crabbe JC, Phillips TJ.	Quantitative trait loci (QTL) applications to substances of abuse: physical dependence studies with nitrous oxide and ethanol in BXD mice	Behav Genet 	23(2)	213-222	Mar	1993 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8512534&dopt=Abstract	8512534		04	100 days			Male			6.06666666666667		12.635		9.53333333333333		0.333333333333333		14.13		4.25		7.81666666666667		15.977				0.806666666666667		8.35		2.47166666666667		0.55		1.04666666666667		3.55						9.33666666666667		4.24333333333333				6.72666666666667		6.44666666666667		7.21333333333333		9.13666666666667		5.57																														12/20/2002			N2OHIC(DIFF)		NDIFFAUC	Nitrous Oxide	gas 75%		JKB		MRG 011002; prior confirmation by JKB with data and publication	8512534.04
Acute ethanol withdrawal-difference from saline,  [Unpublished means from same series of studies as reported in:  Belknap, Metten, Helms, O'Toole, Angeli-Gade, Crabbe & Phillips, 1993 Behav Genetics 23:213-222]		Recombinant inbred (RI) mouse strains were developed primarily as a tool to detect and provisionally map major gene loci--those with effects large enough to cause a bimodal distribution in the trait of interest. This implied that progress toward gene mapping was possible only for gene loci accounting for at least half of the genetic variance. More recently, QTL (quantitative trait loci) approaches have been advanced that do not require bimodal distributions and are thus applicable to a much wider range of phenotypes. They offer the prospect of meaningful progress toward detecting and mapping minor as well as major gene loci affecting any trait of interest, provided there is a significant degree of genetic determination among the RI strains. This paper presents a review of RI gene mapping efforts concerning phenotypes related to drug abuse and presents new data for studies now in progress for nitrous oxide and acute ethanol withdrawal intensity. These two studies exemplify several strengths and limitations of the RI QTL approach.	Belknap JK, Metten P, Helms ML, O'Toole LA, Angeli-Gade S, Crabbe JC, Phillips TJ.	Quantitative trait loci (QTL) applications to substances of abuse: physical dependence studies with nitrous oxide and ethanol in BXD mice	Behav Genet	23(2)	213-222	Mar	1993 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8512534&dopt=Abstract	8512534		05	100 days			Male			5.227		14.08		8.6		9.303		7.9		1.91		3.05		6.27				1.78		5.07		5.6		3.11		6.3		4.06						8.47		5.707				2.21		6.047		6.696		5.5		1.49																														12/20/2002			ETHIC4(DIFF)		DAUC412	EtOH	4 g/kg		JKB		MRG 020402 with JKB	8512534.05
Home cage activity after saline injection		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	01	10-14 wks	70	98	MF	8		13.25		8.375		11.75		8.625		10.75		15.5		11.25		11.375		8.375		7.88888888888889		6		10.75		8		11.875		10.5		12				7.5		11.375		15.75		1.77777777777778		17.125		11.5		7.5		13.5		9.125		8.625		20.75																								6/4/2003	MK Sullivan		SALACT(Home)		ACT0	Saline	Saline	JKBQTL2	JKB	p. 752, Fig 6	MRG 011002 with JKB by publication	8987796.01
Activity-difference from saline for 4 mg/kg methamphetamine [quadrant crossings/min]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	02	10-14 wks	70	98	MF	8	quadrant crossings/min	21.625	2.35	18.7678571428571	4.74	47.25	6.70	35.9305555555556	4.39	41.5	7.43	19.25	8.96	7	5.83	33.125	5.26	8.5	2.54	31.8986111111111	3.39	19.875	3.30	13.125	2.96	35.75	6.70	18.125	8.87	21.875	6.26	31.5	6.26			34.375	4.30	9.5	4.74	10.125	5.52	13.8472222222222	4.17	15.5	7.17	22	6.13	25.5	5.39	33.75	4.65	10.375	5.65	30	4.09	14.75	4.09																							6/4/2003	MK Sullivan		MAACT4		DACT4	Meth	4 mg/kg		JKB	p. 748, Fig 2	MRG 011002 with JKB by publication	8987796.02
Activity-difference from saline for 8 mg/kg methamphetamine [quadrant crossings/min]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	03	10-14 wks	70	98	MF	8	quadrant crossings/min	11.375	3.61	17	5.61	49.875	7.61	24.4861111111111	4.26	43.125	6.70	1.7	5.04	7.25	4.52	14.25	5.78	6.125	4.87	27.4861111111111	3.73	31.5	1.96	15.25	5.13	16.25	7.78	4.375	2.30	16.5	4.43	26.125	8.52			28.7857142857143	4.13	5.5	3.00	-0.875	3.30	25.3472222222222	5.57	9.375	4.17	40.625	7.65	11.5	4.83	12.125	5.57	23.4305555555556	8.96	37.375	4.78	7.375	3.13																							6/4/2003	MK Sullivan		MAACT8		DACT8	Meth	8 mg/kg		JKB	p. 748, Fig 2	MRG 011002 with JKB by publication	8987796.03
Activity-difference from saline for 16 mg/kg methamphetamine [quadrant crossings/min]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	04	10-14 wks	70	98	MF	8	quadrant crossings/min	-8.75	1.89	3.79166666666667	3.96	6.625	9.96	-0.874999999999998	2.39	8.25	4.89	-12.75	1.88	-9.13888888888889	1.14	-2	3.18	-5.75	1.89	-2.88888888888889	3.22	6.875	5.25	3.625	4.89	-7.14285714285714	0.86	-2	3.07	4.875	6.25	-6.85714285714286	1.61			-1.75	2.14	-4.125	3.64	-7.25	2.86	25.4444444444444	4.75	-13.3472222222222	1.64	8	6.75	-1.75	2.46	-7.7	1.57	11.25	3.86	4.25	2.71	-4.25	5.75																							6/4/2003	MK Sullivan		MAACT16		DACT16	Meth	16 mg/kg		JKB	p. 748, Fig 2	MRG 011002 with JKB by publication	8987796.04
Sterotyped chewing responses [N/min]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	05	10-14 wks	70	98	MF	8	N/min	2.25	0.723	8.375	2.349	0	0.400	1.88888888888889	0.979	1.375	1.396	7.3	1.557	8.25	1.830	5.75	2.323	4.875	1.328	5.04166666666667	2.604	0.125	0.145	2.22222222222222	1.149	9.625	2.162	0.875	0.689	4.5	1.430	7.375	2.545			1.44642857142857	0.987	2.875	2.774	3.375	1.174	1.40277777777778	1.277	0	0.289	3.875	2.026	2.275	1.098	2.125	1.226	0.0833333333333333	0.289	2.125	2.145	-0.125	0.366																							6/4/2003	MK Sullivan		MACHEW8		DCHEW8	Meth	8 mg/kg		JKB	p. 748, Fig 3	MRG 011002 with JKB by publication	8987796.05
Change in body temp due to 4 mg/kg methamphetamine [degree C]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	06	10-14 wks	70	98	MF	8	degree C	0.0124999999999957	0.186	-1.00357142857143	0.536	0.832142857142856	0.345	-0.461111111111116	0.299	0.237500000000004	0.206	-3.72499999999999	0.423	-2.05	0.747	0.424999999999997	0.500	0.0625	0.232	0.588888888888889	0.268	-0.18035714285714	0.232	-1.56250000000001	0.742	0.550000000000004	0.495	-1.2125	0.495	0.362499999999997	0.147	-0.137500000000003	0.711			-1.4375	0.232	-0.487499999999997	0.418	-1.8375	0.820	-1.35277777777779	0.340	-0.275000000000006	0.323	-0.737499999999997	0.325	-1.53750000000001	0.691	-0.537500000000001	0.742	-0.279166666666676	0.299	0.125	0.178	-0.76250000000001	0.289																							6/4/2003	MK Sullivan		MATEMP4		DTEMP4	Meth	4 mg/kg		JKB	p. 747, Fig 1	MRG 011002 with JKB by publication	8987796.06
Change in body temp due to 8 mg/kg methamphetamine [degree C]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	07	10-14 wks	70	98	MF	8	degree C	-0.337499999999991	0.254	-0.0875000000000057	0.207	1.3	0.236	0.294444444444444	0.406	0.674999999999997	0.196	-2.3	0.703	-0.762499999999996	0.283	1.1875	0.120	0.225000000000001	0.330	1.02638888888889	0.232	0.357142857142861	0.286	0.799999999999997	0.351	1.77500000000001	0.196	-1.1125	0.083	1.2375	0.402	0.424999999999997	0.283			0.253571428571433	0.428	0.0124999999999957	0.141	-0.63750000000001	0.630	-0.06527777777778	0.601	-0.125000000000007	0.457	0.525000000000006	0.312	-0.850000000000001	0.580	1.3	0.525	-1.26805555555557	0.359	0.824999999999996	0.170	-0.362500000000004	0.417																							6/4/2003	MK Sullivan		MATEMP8		DTEMP8	Meth	8 mg/kg		JKB	p. 747, Fig 1	MRG 011002 with JKB by publication	8987796.07
Change in body temp due to 16 mg/kg methamphetamine [degree C]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains	J Neurosci 	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	08	10-14 wks	70	98	MF	8	degree C	0.162500000000001	0.296	0.258333333333326	0.396	1.05	0.217	1.5375	0.316	1.09499999999999	0.316	-0.149999999999991	0.352	0.680555555555557	0.299	1.40000000000001	0.211	0.75	0.316	1.05138888888889	0.228	0.43214285714285	0.168	0.887499999999996	0.177	1.13035714285714	0.493	1.1875	0.524	1.2625	0.382	1.39821428571428	0.234			1.05	0.359	0.325000000000003	0.239	1.1375	0.274	0.377777777777773	0.353	0.791666666666664	0.217	0.725000000000001	0.328	1.2	0.504	2.3525	0.091	-0.100000000000009	0.202	1.2375	0.316	1.01249999999999	0.140																							6/4/2003	MK Sullivan		MATEMP16		DTEMP16	Meth	16 mg/kg		JKB	p. 747, Fig 1	MRG 011002 with JKB by publication	8987796.08
Morphine consumption-two bottle choice [morphine concentration 0.3 to 0.7 mg/ml]		The use of Recombinant Inbred mouse Strains (RIS) to derive information about the complexity of the genetic architecture underlying various traits is increasing in popularity. Behaviors measured to index sensitivity to drug effects and vulnerability to drug abuse are considered here. Potential uses of RIS are identification of major gene effects, mapping of traits to particular chromosomal sites, determining genetic correlations between characters, and identifying behaviorally extreme genotypes. This approach has led to identification of a major gene moderating alcohol acceptance in mice and has revealed a more complex polygenic system influencing morphine consumption.	Phillips TJ, Belknap JK, Crabbe JC.	Use of recombinant inbred strains to assess vulnerability to drug abuse at the genetic level	J Addict Dis 	10(1-2)	73-87		1991		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2065120&dopt=Abstract	2065120		01				Male			157		16		16		42		84		50		27		27				97		29		23		148		16		17						19		96		19		99		52		71		49		97																														12/20/2002			MORCONS		MORCON	Morphine	mg/kg/day		JKB	p. 80, Table 1	MRG 020402 with JKB by publication	2065120.01
Quinine consumption-two bottle choice [quinine concentration 0.1 to 0.4 mg/ml]		The use of Recombinant Inbred mouse Strains (RIS) to derive information about the complexity of the genetic architecture underlying various traits is increasing in popularity. Behaviors measured to index sensitivity to drug effects and vulnerability to drug abuse are considered here. Potential uses of RIS are identification of major gene effects, mapping of traits to particular chromosomal sites, determining genetic correlations between characters, and identifying behaviorally extreme genotypes. This approach has led to identification of a major gene moderating alcohol acceptance in mice and has revealed a more complex polygenic system influencing morphine consumption.	Phillips TJ, Belknap JK, Crabbe JC.	Use of recombinant inbred strains to assess vulnerability to drug abuse at the genetic level	J Addict Dis 	10(1-2)	73-87		1991		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2065120&dopt=Abstract	2065120		02				Male			36		24		32		12		135		20		13		10				11		17		17		62		5		27						11		9		19		58		85		25		39		88																														12/20/2002			QUINCONS		QUINCON	Quinine	mg/kg/day		JKB	p. 80, Table 1	MRG 020402 with JKB by publication	2065120.02
Saccharin preference 	Saccharin preference - mean of 2 studies;Unpublished means from same series of studies as reported in:  1) Phillips, Belknap, Crabbe 1991, J Addictive Diseases 10:73-87;  2) Belknap, Metten, Helms, O'toole, Angeli-Gade, Crabbe & Phillips, 1993 Behav Genetics 23:213-222	The use of Recombinant Inbred mouse Strains (RIS) to derive information about the complexity of the genetic architecture underlying various traits is increasing in popularity. Behaviors measured to index sensitivity to drug effects and vulnerability to drug abuse are considered here. Potential uses of RIS are identification of major gene effects, mapping of traits to particular chromosomal sites, determining genetic correlations between characters, and identifying behaviorally extreme genotypes. This approach has led to identification of a major gene moderating alcohol acceptance in mice and has revealed a more complex polygenic system influencing morphine consumption.	Phillips TJ, Belknap JK, Crabbe JC.	Use of recombinant inbred strains to assess vulnerability to drug abuse at the genetic level	J Addict Dis 	10(1-2)	73-87		1991		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2065120&dopt=Abstract	2065120		97				Male			0.95		0.715		0.79		0.765		0.915		0.9		0.715		0.695				0.765		0.6675		0.805		0.86		0.77		0.765						0.615		0.641		0.84		0.8965		0.717		0.7255		0.873		0.79																														12/19/2002			SACCPREF		SACCPREF	Saccharin	preference ratio		JKB		MRG 020402 with JKB	2065120.97
Saccharin consumption 	Saccharin consumption - mean of 2 studiesUnpublished means from same series of studies as reported in:  1) Phillips, Belknap, Crabbe 1991, J Addictive Diseases 10:73-87;  2) Belknap, Metten, Helms, O'Toole, Angeli-Gade, Crabbe & Phillips, 1993 Behav Genetics 23:213-222	The use of Recombinant Inbred mouse Strains (RIS) to derive information about the complexity of the genetic architecture underlying various traits is increasing in popularity. Behaviors measured to index sensitivity to drug effects and vulnerability to drug abuse are considered here. Potential uses of RIS are identification of major gene effects, mapping of traits to particular chromosomal sites, determining genetic correlations between characters, and identifying behaviorally extreme genotypes. This approach has led to identification of a major gene moderating alcohol acceptance in mice and has revealed a more complex polygenic system influencing morphine consumption.	Phillips TJ, Belknap JK, Crabbe JC.	Use of recombinant inbred strains to assess vulnerability to drug abuse at the genetic level	J Addict Dis 	10(1-2)	73-87		1991		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2065120&dopt=Abstract	2065120		96				Male			806.5		383		352		459.5		1178.5		544.5		342		343				410.5		258.5		528		484		353.5		410						332.5		261.5		417.5		442.5		453.5		365		472		536.5																														12/19/2002			SACCONS		SACCCON	Saccharin	mg/kg/day		JKB		MRG 020402 with JKB	2065120.96
Locomotor activity post cocaine (32 mg/kg) [activity counts/hr]		The present study investigated the effects of acute and repeated administration of cocaine (1.0-56.0 mg/kg) on locomotor activity in the genetically distinct DBA/2J and C57BL/6J inbred strains of mice. In addition, quantitative trait loci analysis of the effects of acute and repeated cocaine in 16 BXD recombinant inbred strains was used to provisionally detect and map minor gene loci which associate with cocaine responsiveness. Whereas locomotor activity was elevated maximally in both strains by 32 mg/kg of cocaine, DBA/2J mice were stimulated to a much greater extent than C57BL/6J mice. The stimulant effects of cocaine were diminished to control levels in DBA/2J mice after repeated daily injections, whereas cocaine-induced locomotion remained consistent in C57BL/6J mice throughout the 7-day testing period. Emergence of stereotyped behavior with repeated daily injections of 32 mg/kg of cocaine was observed in DBA/2J but not C57BL/6J mice. No differences in brain cocaine levels were found between the DBA/2J and C57BL/6J strains after acute or repeated injections. Quantitative trait loci analysis indicated significant associations of differences in cocaine responsiveness with marker loci on several chromosomes in the BXD recombinant inbred series. Those marker loci associated with the acute cocaine response were in most cases different from those markers associated with long-term responses. The current results demonstrate that genotype-dependent variation exists in behavioral responsiveness to cocaine in mice and suggest that the acute and long-term responses to cocaine may be under the control of separate sets of genes.	Tolliver BK, Belknap JK, Woods WE, Carney JM.	Genetic analysis of sensitization and tolerance to cocaine	J Pharmacol Exp Ther	270(3)	1230-1238	Sep	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7932176&dopt=Abstract	7932176		01				Male	3-8	activitycounts/hr 	1481	89.0	2470	210.3					1814	239.1			2574	251.7			1557	134.3			1622	83.0	1333	69.4	1995	217.4	1787	73.8							2345	83.3	1702	88.7	1383	165.4			2158	112.0	1539	129.6	1494	189.3			1771	117.6	1597	115.8	1909	166.4																							6/26/2003	MK Sullivan		COCACT32		COACT	Cocaine	32 mg/kg		Tolliver/JKB	p. 1235, Fig 6	MRG 011002 with JKB by publication	7932176.01
Sensitization of locomotor response to cocaine (32 mg/kg) [% initial response]		The present study investigated the effects of acute and repeated administration of cocaine (1.0-56.0 mg/kg) on locomotor activity in the genetically distinct DBA/2J and C57BL/6J inbred strains of mice. In addition, quantitative trait loci analysis of the effects of acute and repeated cocaine in 16 BXD recombinant inbred strains was used to provisionally detect and map minor gene loci which associate with cocaine responsiveness. Whereas locomotor activity was elevated maximally in both strains by 32 mg/kg of cocaine, DBA/2J mice were stimulated to a much greater extent than C57BL/6J mice. The stimulant effects of cocaine were diminished to control levels in DBA/2J mice after repeated daily injections, whereas cocaine-induced locomotion remained consistent in C57BL/6J mice throughout the 7-day testing period. Emergence of stereotyped behavior with repeated daily injections of 32 mg/kg of cocaine was observed in DBA/2J but not C57BL/6J mice. No differences in brain cocaine levels were found between the DBA/2J and C57BL/6J strains after acute or repeated injections. Quantitative trait loci analysis indicated significant associations of differences in cocaine responsiveness with marker loci on several chromosomes in the BXD recombinant inbred series. Those marker loci associated with the acute cocaine response were in most cases different from those markers associated with long-term responses. The current results demonstrate that genotype-dependent variation exists in behavioral responsiveness to cocaine in mice and suggest that the acute and long-term responses to cocaine may be under the control of separate sets of genes.	Tolliver BK, Belknap JK, Woods WE, Carney JM.	Genetic analysis of sensitization and tolerance to cocaine	J Pharmacol Exp Ther	270(3)	1230-1238	Sep	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7932176&dopt=Abstract	7932176		02				Male	3-8	% initial response	81.4		28.2						92.5				71.7				111.4				128.7		97.1		53.1		115.0								59		81.3		100				87.4		86.4		102.0				102		88.6		90																								6/26/2003	MK Sullivan		COCSEN32		COSENSIT	Cocaine	32 mg/kg		Tolliver/JKB	p. 1235, Fig 6	MRG 011002 with JKB by publication	7932176.02
Body weight [g]		Adult C57BL/6J (B6) male mice had 37% heavier brains than did DBA/2J (D2) mice, while their body weights did not differ. The BXD recombinant inbred (RI) series of 20 strains, derived from a cross between B6 and D2 inbred strains, was used as the initial screen to determine significant associations between male brain weight and brain:body weight ratio, with allelic variation at 360 known marker gene loci. For brain weight, this yielded five candidate chromosome regions, each reflecting a possible quantitative trait locus (QTL) site affecting brain weight. The second step was to test as many of these five as possible using standard (non-RI) inbred strain data for brain weight previously reported in the literature. For this purpose, only strains possessing the same alleles as the B6 or D2 strains were used. Sufficient data to test two of the five candidate QTL were available. Of these, one was strongly supported as a site affecting brain weight--the D7rp2 region of chromosome 7. For the brain to body weight ratio, four chromosome regions emerged as significantly associated in the BXD series, but none were amenable to testing due to a lack of allelic information for the standard inbred strains. However, two of these regions showed highly significant associations (p less than 0.001, single test) that merit consideration as QTL sites for future testing. These two are the Hba region on chromosome 11 and the D17Tu7 region on chromosome 17. The genetic correlation between brain and body weight was low (r = 0.28), indicating that these two traits are largely genetically independent in the BXD RI series.	Belknap JK, Phillips TJ, O'Toole LA.	Quantitative trait loci associated with brain weight in the BXD/Ty recombinant inbred mouse strains	Brain Res Bul 	29(3-4)	337-344	Sept-Oct	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1393606&dopt=Abstract	1393606		01	11-13 wks	77	91	Male	7-8	g	25.5	1.71	25.5	2.08	27.6	1.60	28.4	1.84	26.1	1.84	25	2.00	26.4	1.25	27.1	1.64			25.2	0.96	29.3	1.75	30.4	1.60	27.8	1.54	26.75	1.91	29	2.56					28.4	3.26	25.1	0.79	24.3	2.42	25	1.66	24.7	2.17	25.2	2.06	26.3	1.83	24.7	2.23																													6/24/2003	MK Sullivan		BODYWGT		BODWGT			BODYWGT	JKB	p. 340, Table 1	MRG 011002 with JKB by publication	1393606.01
Brain weight [mg]		Adult C57BL/6J (B6) male mice had 37% heavier brains than did DBA/2J (D2) mice, while their body weights did not differ. The BXD recombinant inbred (RI) series of 20 strains, derived from a cross between B6 and D2 inbred strains, was used as the initial screen to determine significant associations between male brain weight and brain:body weight ratio, with allelic variation at 360 known marker gene loci. For brain weight, this yielded five candidate chromosome regions, each reflecting a possible quantitative trait locus (QTL) site affecting brain weight. The second step was to test as many of these five as possible using standard (non-RI) inbred strain data for brain weight previously reported in the literature. For this purpose, only strains possessing the same alleles as the B6 or D2 strains were used. Sufficient data to test two of the five candidate QTL were available. Of these, one was strongly supported as a site affecting brain weight--the D7rp2 region of chromosome 7. For the brain to body weight ratio, four chromosome regions emerged as significantly associated in the BXD series, but none were amenable to testing due to a lack of allelic information for the standard inbred strains. However, two of these regions showed highly significant associations (p less than 0.001, single test) that merit consideration as QTL sites for future testing. These two are the Hba region on chromosome 11 and the D17Tu7 region on chromosome 17. The genetic correlation between brain and body weight was low (r = 0.28), indicating that these two traits are largely genetically independent in the BXD RI series.	Belknap JK, Phillips TJ, O'Toole LA.	Quantitative trait loci associated with brain weight in the BXD/Ty recombinant inbred mouse strains	Brain Res Bul 	29(3-4)	337-344	Sept-Oct	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1393606&dopt=Abstract	1393606		02	11-13 wks	77	91	Male	7-8	mg	465	23	339	19	450	22	390	19	477	27	361	16	421	13	419	15			412	13	403	9	439	9	429	14	436	16	427	13					409	20	431	10	432	30	380	17	394	16	381	18	389	20	375	11																													6/24/2003	MK Sullivan		BRAINWGT		BRAINWGT			BRAINWGT	JKB	p. 340, Table 1	MRG 011002 with JKB by publication	1393606.02
Cocaine in mg/kg (infused via tail vein) to   induce tonic seizure  [mg/kg]		Seizures are a well known consequence of human cocaine abuse, and in rodent models, sensitivity to cocaine seizures has been shown to be strongly influenced by genotype. For example, several studies have reported significant differences between the C57BL/6 (B6) and DBA/2 (D2) inbred mouse strains in their sensitivity to cocaine-induced seizures. This prompted our use of the BXD recombinant inbred (RI) strain set and an F(2) population derived from the B6 and D2 progenitor strains for further genetic analyses and for gene mapping efforts in this study. Cocaine was infused into the lateral tail vein, and the doses needed to induce a running bouncing clonic seizure and a tonic hindlimb extensor seizure were recorded for each mouse. In the BXD RI set, a genome-wide search was carried out for QTLs (quantitative trait loci), which are sites on a chromosome containing genes that influence seizure susceptibility. An F(2) population (B6D2F2, n = 408) was subsequently used as a second, confirmation step. Based on both RI and F(2) results, three QTLs emerged as significant (P <.00005): one for clonic seizures on chromosome 9 (distal), and two for tonic seizures on chromosomes 14 (proximal to mid) and 15 (distal). Two additional QTLs emerged as suggestive (P <.0015), both associated with clonic seizures on chromosomes 9 (proximal) and 15 (distal). Both QTLs on chromosome 9 were sex-specific, with much larger effects on the phenotype seen in females than in males.	Hain HS, Crabbe JC,       Bergeson SE, Belknap JK. 	Cocaine-induced seizure thresholds: quantitative trait loci detection and mapping in two populations derived from the C57BL/6 and DBA/2 mouse strains	J Pharmacol Exp Ther	293(1)	180-187	Apr	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10734168&dopt=Abstract	10734168		01	56-100 days 	56	100	Female	7-16	mg/kg	36.5092843340253	1.05	45.8623787362414	1.15	42.9703626911218	1.99	46.3609349736889	1.81	43.4960099553144	3.05	48.0771280463759	2.93	44.6149206926665	2.06	38.9730137289765	1.64	48.6677557555129	1.60	39.5212449334861	1.03	39.4036744928305	1.27	39.9767680020278	1.74	37.3012008962622	1.55	43.3300328369933	1.78	39.4037704331372	1.18	45.4332262655791	1.24			35.9427625388382	1.01	49.5509290179926	2.94			38.7927845701966	1.48	46.6208980595439	3.05	38.7701207182665	1.08	38.7466553026451	1.64	44.3891465498985	2.56	42.0057332089545	1.24	34.0522375511561	0.70	44.0018244149537	1.59																							6/4/2003	MK Sullivan	MK Sullivan	COCTON		MGKGTON	Cocaine	1mg/ml	RI-166	JKB/JCC	p. 182, Fig.1 top	JD 121301  from publication	10734168.01
Cocaine in mg/kg (infused via tail vein) to induce clonic seizure [mg/kg]                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            		Seizures are a well known consequence of human cocaine abuse, and in rodent models, sensitivity to cocaine seizures has been shown to be strongly influenced by genotype. For example, several studies have reported significant differences between the C57BL/6 (B6) and DBA/2 (D2) inbred mouse strains in their sensitivity to cocaine-induced seizures. This prompted our use of the BXD recombinant inbred (RI) strain set and an F(2) population derived from the B6 and D2 progenitor strains for further genetic analyses and for gene mapping efforts in this study. Cocaine was infused into the lateral tail vein, and the doses needed to induce a running bouncing clonic seizure and a tonic hindlimb extensor seizure were recorded for each mouse. In the BXD RI set, a genome-wide search was carried out for QTLs (quantitative trait loci), which are sites on a chromosome containing genes that influence seizure susceptibility. An F(2) population (B6D2F2, n = 408) was subsequently used as a second, confirmation step. Based on both RI and F(2) results, three QTLs emerged as significant (P <.00005): one for clonic seizures on chromosome 9 (distal), and two for tonic seizures on chromosomes 14 (proximal to mid) and 15 (distal). Two additional QTLs emerged as suggestive (P <.0015), both associated with clonic seizures on chromosomes 9 (proximal) and 15 (distal). Both QTLs on chromosome 9 were sex-specific, with much larger effects on the phenotype seen in females than in males.	Hain HS, Crabbe JC,  Bergeson SE, Belknap JK. 	Cocaine-induced seizure thresholds: quantitative trait loci detection and mapping in two populations derived from the C57BL/6 and DBA/2 mouse strains	J Pharmacol Exp Ther	293(1)	180-187	Apr	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10734168&dopt=Abstract	10734168		02	56-100 days 	56	100	Female	7-16	mg/kg	21.1275869781027	0.75	21.903677521797	1.59	24.3794503374416	3.26	21.8333066738383	2.18	21.6786293001535	2.46	20.1582397852819	1.24	23.9731186492713	1.45	21.8606255012244	1.83	24.867635937228	1.55	17.5034216551746	1.22	21.7689514914138	0.99	21.8178716923466	1.76	17.4457084496112	1.71	20.1131869961416	1.18	24.3516411928639	1.45	23.4871948042632	1.45			20.3500609275227	1.01	23.5815221713196	2.51			20.7144960755053	1.72	22.1648480352814	2.23	22.8863072036995	1.95	19.6430463704733	1.43	20.8623671215829	1.66	22.8056520761417	1.66	20.1509430417039	1.20	20.7370448138035	0.98																							6/4/2003	MK Sullivan	MK Sullivan           	COCCLO		MGKGCLO	Cocaine	1mg/ml	RI-166	JKB/JCC	p. 182, Fig.1 bottom	JD 121301  from publication	10734168.02
Acute ethanol activity response - Difference between experimental 2g/kg ip EtOH and saline control group [activity counts/min]		Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL 	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	01	56-125 days	56	125	Male	13-34	activity counts/min	28.869	8.34	75.200	8.27	42.207	8.30	20.144	4.90	36.412	2.44	15.49	3.92	85.832	4.97	49.069	4.57	52.4	6.92	2.147	4.90	43.093	4.50	58.071	6.34	18.172	2.91	15.048	2.78	44.434	7.15					50.538	5.53	33.052	5.00			28.221	3.84	68.007	9.87	38.566	10.60	23.353	4.77	31.488	5.05																													7/3/2003	MK Sullivan		ETSALACT(C1DIFF)	Figure 1 data; also EtOH: Act in Tables 4-5	E1MS1; C1	EtOH	2 g/kg	CPP-59	CLC	Fig 1; Tables 4-5	MRG 120601 from publication	7480533.01
Within-subject tolerance/sensitization to ethanol effects on locomotor activity (i.e., 4th ethanol trial activity minus 1st ethanol trial activity)		Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology 	120(1)	28-41	July	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	02	56-125 days	56	125	Male			-59.094		26.921		-44.237		-26.048		-22.375		-47.387		-10.206		15.869		-37.031		-23.027		-19.28		-30.107		-15.159		-29.042		-1.931						10.117		-2.704				7.3		-34.855		34.772		-15.973		-4.218																														12/20/2002			ETSEN (C4C1)	SENS1: ACT	E4ME1	EtOH	2 g/kg	CPP-59	CLC	means not in paper; analyzed in Tables 4-5	MRG 120601 from publication	7480533.02
Ethanol induced conditioned place preference - Time on EtOH paired floor during 30 min test [%]		Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL 	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	03	56-125 days	56	125	Male	6-16	%	58.316	2.38	59.618	3.38	65.087	3.56	62.43	3.56	54.588	2.58	63.214	2.80	59.001	2.26	60.163	2.01	78.344	3.80	57.973	2.87	59.701	2.74	55.239	2.54	64.039	2.92	61.564	5.14	57.696	1.98					49.491	1.80	65.529	5.04			74.6	3.32	49.865	2.18	66.859	4.08	54.526	3.50	53.349	1.99																													7/2/2003	MK Sullivan		ETCPP	PREF	PDT30	EtOH	2 g/kg	CPP-59	CLC	p. 33, Fig 2	JD 010302 from publication	7480533.03
Within-subject habituation (i.e., 4th saline trial activity minus 1st saline activity trial activity)	[Unpublished means from same series of studies as reported in:    Cunningham 1995 PsychoPharm 120:28-41]	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	95	56-125 days	56	125	Male			-47.925		-10.243		-37.8		-36.568		-13.088		-41.865		-18.465		-20.793		-21.569		-32.167		-22.473		-23.9		-8.386		-17.503		-14.676						-6.034		-11.252				-6.357		-32.848		-26.041		-14.067		-18.888																														12/19/2002			SALACT(C4C1)		S4MS1	Saline		CPP-59	CLC		JD 010302 from publication	7480533.95
Acute Locomotor Activity Response to 2 g/kg i.p. EtOH on 11th day in chronic saline injected mice, 1- 5 minutes after injection [cm]		Investigations of ethanol's (EtOH's) complex response profile, including locomotor and other effects, are likely to lead to a more in-depth understanding of the constituents of alcohol addiction. Locomotor activity responses to acute and repeated EtOH (2 g/kg, i.p) exposures were measured in BXD recombinant inbred (RI) mice and their C57BL/6J (B6) and DBA/2J (D2) progenitors. Both the acute response and the change in initial EtOH response with repeated treatments were strain-dependent. The coefficient of genetic determination was 0.38-0.49 for initial locomotor response to EtOH, and 0.29 for change in response. Changes in response were largely attributable to sensitization of locomotor stimulation. Quantitative trait loci (QTL) analyses identified significant marker associations with basal activity, acute locomotor response, and change in response. Markers were for QTL on several chromosomes, and there was only one case of overlap in marker associations among phenotypes. Acute locomotor response and locomotor sensitization were negatively correlated with 3% EtOH preference drinking data collected in BXD RI strains. Overall, these results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.	Phillips TJ, Huson M, Gwiazdon C, Burkhart-Kasch S, Shen EH.	Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice	Alcohol Clin Exp Res	19(2)	269-278.	Apr	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625557&dopt=Abstract	7625557	95351511	01	7-19 wks	49	133	Female		Horizontal Distance traveled cm 	546		973		-241		725		-208		-493		1185		358		921		387		662		813		-266		38		726						1074		454		996		194		1242		837		529		309																														12/27/2002			ETACT2(CS)	ACCS	CS5D11D2	EtOH	2 g/kg	RI-58	TJP	Figure 1 inset y-axis, p. 273	MRG 010202 with TJP from publication and data file	7625557.01
Ethanol Locomotor Sensitization Between Group: Acute Response to 2 g/kg EtOH, Day 11 Locomotor Activity Difference (Chronic EtOH minus Chronic Saline), 1-5 minutes after injection [cm] 		Investigations of ethanol's (EtOH's) complex response profile, including locomotor and other effects, are likely to lead to a more in-depth understanding of the constituents of alcohol addiction. Locomotor activity responses to acute and repeated EtOH (2 g/kg, i.p) exposures were measured in BXD recombinant inbred (RI) mice and their C57BL/6J (B6) and DBA/2J (D2) progenitors. Both the acute response and the change in initial EtOH response with repeated treatments were strain-dependent. The coefficient of genetic determination was 0.38-0.49 for initial locomotor response to EtOH, and 0.29 for change in response. Changes in response were largely attributable to sensitization of locomotor stimulation. Quantitative trait loci (QTL) analyses identified significant marker associations with basal activity, acute locomotor response, and change in response. Markers were for QTL on several chromosomes, and there was only one case of overlap in marker associations among phenotypes. Acute locomotor response and locomotor sensitization were negatively correlated with 3% EtOH preference drinking data collected in BXD RI strains. Overall, these results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.	Phillips TJ, Huson M, Gwiazdon C, Burkhart-Kasch S, Shen EH.	Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice	Alcohol Clin Exp Res	19(2)	269-278.	Apr	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625557&dopt=Abstract	7625557	95351511	02	7-19 wks	49	133	Female		Horizontal Distance traveled cm 	-694		-134		-468		507		435		395		-558		663		456		-372		1226		275		176		1026		1065						696		-62		758		935		430		388		677		356																														12/27/2002			ETSEN2(BG)	deltaBG	BGSENS5M	EtOH	2 g/kg	RI-58	TJP	Figure 2 inset y-axis, p. 273	MRG 010202 with TJP from publication and data file	7625557.02
Ethanol Locomotor Sensitization Within Group: Change in locomotor response, 1 - 5 minutes after 2 g/kg EtOH injection (i.p) after repeated treatment; Day 11 (fifth EtOH treatment) minus Day 3 (first EtOH treatment) for the chronic EtOH group [cm]		Investigations of ethanol's (EtOH's) complex response profile, including locomotor and other effects, are likely to lead to a more in-depth understanding of the constituents of alcohol addiction. Locomotor activity responses to acute and repeated EtOH (2 g/kg, i.p) exposures were measured in BXD recombinant inbred (RI) mice and their C57BL/6J (B6) and DBA/2J (D2) progenitors. Both the acute response and the change in initial EtOH response with repeated treatments were strain-dependent. The coefficient of genetic determination was 0.38-0.49 for initial locomotor response to EtOH, and 0.29 for change in response. Changes in response were largely attributable to sensitization of locomotor stimulation. Quantitative trait loci (QTL) analyses identified significant marker associations with basal activity, acute locomotor response, and change in response. Markers were for QTL on several chromosomes, and there was only one case of overlap in marker associations among phenotypes. Acute locomotor response and locomotor sensitization were negatively correlated with 3% EtOH preference drinking data collected in BXD RI strains. Overall, these results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.	Phillips TJ, Huson M, Gwiazdon C, Burkhart-Kasch S, Shen EH.	Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice	Alcohol Clin Exp Res	19(2)	269-278.	Apr	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625557&dopt=Abstract	7625557	95351511	03	7-19 wks	49	133	Female		Horizontal Distance traveled cm 	-318	124	-725	350	-866	200	260	289	279	117	-51	223	-1013	488	1060	303	726	492	-297	303	644	309	-46	231	365	188	433	242	1119	309					682	427	39	242	1125	293	899	175	252	203	402	270	586	298	192	266																													7/2/2003	MK Sullivan		ETSEN2(CD)	deltaCD	D11D35M	EtOH	2 g/kg	RI-58	TJP	Figure 2 and Figure 2 inset x-axis, p. 273	MRG 010202 with TJP from publication and data file	7625557.03
Acute locomotor response, 1 to 5 minutes after 2g/kg i.p. EtOH in chronic ethanol sensitized mice [cm] 		Investigations of ethanol's (EtOH's) complex response profile, including locomotor and other effects, are likely to lead to a more in-depth understanding of the constituents of alcohol addiction. Locomotor activity responses to acute and repeated EtOH (2 g/kg, i.p) exposures were measured in BXD recombinant inbred (RI) mice and their C57BL/6J (B6) and DBA/2J (D2) progenitors. Both the acute response and the change in initial EtOH response with repeated treatments were strain-dependent. The coefficient of genetic determination was 0.38-0.49 for initial locomotor response to EtOH, and 0.29 for change in response. Changes in response were largely attributable to sensitization of locomotor stimulation. Quantitative trait loci (QTL) analyses identified significant marker associations with basal activity, acute locomotor response, and change in response. Markers were for QTL on several chromosomes, and there was only one case of overlap in marker associations among phenotypes. Acute locomotor response and locomotor sensitization were negatively correlated with 3% EtOH preference drinking data collected in BXD RI strains. Overall, these results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.	Phillips TJ, Huson M, Gwiazdon C, Burkhart-Kasch S, Shen EH.	Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice	Alcohol Clin Exp Res	19(2)	269-278.	Apr	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625557&dopt=Abstract	7625557	95351511	04	7-19 wks	49	133	Female		Horizontal Distance traveled cm 	84	114	1521	263	268	265	843	100	-174	95	-36	138	1587	358	-162	174	924	396	504	168	976	200	1157	243	-204	121	649	159	675	187					1026	284	163	124	644	210	45	87	1445	189	891	181	747	193	382	143																													7/2/2003	MK Sullivan		ETACT2(CD)	ACCD	D3D25M	EtOH	2 g/kg	RI-58	TJP	Figure 1 and Figure 1 inset x-axis, p. 273	MRG 010202 with TJP from publication and data file	7625557.04
Locomotor Activity Day 2, 1 - 5 minutes after saline i.p. [cm]		Investigations of ethanol's (EtOH's) complex response profile, including locomotor and other effects, are likely to lead to a more in-depth understanding of the constituents of alcohol addiction. Locomotor activity responses to acute and repeated EtOH (2 g/kg, i.p) exposures were measured in BXD recombinant inbred (RI) mice and their C57BL/6J (B6) and DBA/2J (D2) progenitors. Both the acute response and the change in initial EtOH response with repeated treatments were strain-dependent. The coefficient of genetic determination was 0.38-0.49 for initial locomotor response to EtOH, and 0.29 for change in response. Changes in response were largely attributable to sensitization of locomotor stimulation. Quantitative trait loci (QTL) analyses identified significant marker associations with basal activity, acute locomotor response, and change in response. Markers were for QTL on several chromosomes, and there was only one case of overlap in marker associations among phenotypes. Acute locomotor response and locomotor sensitization were negatively correlated with 3% EtOH preference drinking data collected in BXD RI strains. Overall, these results demonstrate locomotor sensitization induced by EtOH, suggest independence of genetic determination of locomotor responses to acute and repeated EtOH exposure, and partially support a relationship between reduced sensitivity to the locomotor stimulant/sensitizing effects of EtOH and EtOH consumption.	Phillips TJ, Huson M, Gwiazdon C, Burkhart-Kasch S, Shen EH.	Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice	Alcohol Clin Exp Res	19(2)	269-278.	Apr	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625557&dopt=Abstract	7625557	95351511	05	7-19 wks	49	133	Female		Horizontal Distance traveled cm 	1447		1362		1661		1528		1086		1162		886		1845		573		1643		1175		1729		1171		1035		2014						1411		949		1264		823		1360		1074		899		2146																														12/27/2002			SALACT(5MIN)	BASACT5	SAL5M	Saline		RI-58	TJP	Basis for QTL analysis of basal activity, p. 272 Table 2	MRG 010202 with TJP from publication and data file	7625557.05
Consumption of 0.2% saccharin (mg/kg) vs. tap water; means of days 2 and 4 of a 4-day 24-hr access period [g/kg/day]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		01	51-125 days	51	125	Female	10-18	g/kg/day	853.935	111.717	471.707	73.838			250.743	80.303	748.408	168.939	787.394	43.939			330.42	58.485			343.077	57.980	420.033	54.495	537.171	90.909	652.835	72.576	415.414	47.879	412.785	59.596	639.584	75.253			533.912	23.333			438.621	105.001	674.217	92.980	807.822	70.152	534.837	58.434			1071.038	88.637			591.661	116.768	572.167	55.012																							7/11/2003	MK Sullivan		SACCONS0.2(%)	0.2%SacCon	AVSACCON	Saccharin	0.002	RI-72	TJP	p. 935, Fig. 2	MRG 010202 with TJP from publication and data file	7978106.01
Consumption of 3% Ethanol (g/kg) vs. tap water; means of days 2 and 4 of a 4-day 24-hr access period [g/kg/day]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		02	51-125 days	51	125	Female	10-18	g/kg/day	3.538	0.557	0.279	0.264			2.052	0.841	1.669	0.734	2.086	0.417			0.981	0.301			2.765	0.446	0.438	0.286	0.906	0.374	3.578	0.657	2.218	0.539	0.951	0.341	2.975	0.403			0.967	0.516			1.64	0.786	0.614	0.246	1.741	0.551	2.159	0.821			2.795	0.517			2.658	0.601	0.819	0.429																							7/11/2003	MK Sullivan		ETCONS3(%)	3%EtOHCon	AV3EG	EtOH	0.03	RI-72	TJP	p. 934, Fig.1	MRG 010202 with TJP from publication and data file	7978106.02
Consumption of 3% Ethanol (g/kg) in 0.2% saccharin vs. tap water; means of days 2 and 4 of a 4-day 24-hr access period [g/kg/day]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		03	51-125 days	51	125	Female	10-18	g/kg/day	10.965	0.635	2.000	0.721			6.135	0.833	11.207	1.051	7.023	0.829			2.924	0.633			4.828	0.424	6.245	1.666	6.159	0.945	7.236	0.875	5.58	0.563	3.274	0.845	5.534	0.614			5.473	0.547			11.658	0.719	6.992	0.630	8.083	0.547	6.646	0.766			10.266	0.896			7.308	1.060	4.638	0.980																							7/11/2003	MK Sullivan		ETSACCONS3(%)	3%EtOH/SacCon	AV3SG	EtOH	0.03	RI-72	TJP	p. 935, Fig. 2	MRG 010202 with TJP from publication and data file	7978106.03
Consumption of 10% Ethanol (g/kg) in tap water offered vs. tap water; means are the average of days 2 and 4 of a 4-day 24-hr access period [g/kg/day]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		04	51-125 days	51	125	Female	10-18	g/kg/day	10.562	1.319	1.306	0.981			6.084	1.505	5.506	1.192	4.425	1.008			0.601	0.012			2.759	0.918	0.687	0.411	1.741	0.613	5.836	1.210	4.849	1.407	0.364	0.105	2.477	0.916			2.589	1.017			2.203	1.032	2.417	0.805	2.024	0.706	6.658	0.903			2.466	0.901			8.096	1.403	1.28	0.905																							7/11/2003	MK Sullivan		ETCONS10(%)	10%EtOHCon	AV10EG	EtOH	0.1	RI-72	TJP	p. 934, Fig.1	MRG 010202 with TJP from publication and data file	7978106.04
Consumption of 10% Ethanol (g/kg) in 0.2% saccharin and tap water offered vs. tap water; means of days 2 and 4 of a 4-day 24-hr access period [g/kg/day]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		05	51-125 days	51	125	Female	10-18	g/kg/day	18.194	1.847	1.05	0.660			11.378	1.216	13.58	1.435	12.161	1.241			1.98	0.637			6.256	1.020	6.588	2.212	5.727	1.120	14.376	0.540	11.1	1.626	3.678	1.112	6.692	1.543			8.083	1.528			15.58	1.78	10.256	0.747	10.05	0.235	12.975	1.642			13.02	1.740			12.737	0.871	4.135	1.568																							7/11/2003	MK Sullivan		ETSACCONS10(%)	10%EtOH/SacCon	AV10SG	EtOH	0.1	RI-72	TJP	p. 935, Fig. 2	MRG 010202 with TJP from publication and data file	7978106.05
Corrected area under the Ethanol withdrawal curve; mice were assessed for handling-induced convulsions after voluntary ethanol consumption.		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		06	51-125 days	51	125	Female	10-18		5.66		2.61				0.52		2.18		5.69				0.6				1.64		1.05		1.17		3.21		4.68		0.48		0				4.82				1.26		1.75		2.33		3.3				3.42				0.31		1.5																								12/20/2002			ETHIC	EtOHWD	COAUC	EtOH	0.1	RI-72	TJP	p.938, Table 2	MRG 010202 with TJP from publication and data file	7978106.06
Preference for 10% Ethanol (g/kg) in tap water offered vs. tap water; means are the average of days 2 and 4 of a 4-day 24-hr access period.		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		07	51-125 days	51	125	Female	10-18		0.554		0.086				0.32		0.35		0.251				0.051				0.168		0.045		0.061		0.356		0.302		0.024		0.167				0.146				0.127		0.265		0.171		0.428				0.14				0.488		0.112																								12/20/2002			ETPREF10(%)	10%EtOHPref	PR10E	EtOH	0.1	RI-72	TJP	p. 934, Fig.1	MRG 010202 with TJP from publication and data file	7978106.07
Locomotor response (photocell beam interruptions) to acute 2 g/kg i.p Ethanol injection; Day 3 (first Ethanol treatment) minus Day 2 (saline baseline) in the chronic EtOH group; 10 min activity test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR. 	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		01				Female			-18		151		96		350		-227		-401		88				188		-128		353		79		78		-67		269		541				562		-117		-37		-44		241		608		-23		58		947		-142		-345																								12/20/2002			ETACT2(GRIDCD)		ACTD3D2	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 2 top	MRG 010202 with TJP from publication and data file	8627538.01
Locomotor response (photocell beam interruptions) to acute 2 g/kg Ethanol injection (i.p); Day 11 (only Ethanol treatment) minus Day 2 (saline baseline) in the chronic saline (CS) group; 10 min activity test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		02				Female			-105		272		68		304		-426		-443		170				262		33		524		-68		3		-214		213		780				428		8		-23		79		247		687		-30		538		979		-13		-379																								12/20/2002			ETACT2(GRIDCS)		ACTD11D2	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 2 top inset	MRG 010202 with TJP from publication and data file	8627538.02
Change in locomotor response (photocell beam interruptions) to 2 g/kg i.p EtOH injection (i.p) after repeated treatment; Day 11 (fifth EtOH treatment) minus Day 3 (first EtOH treatment) in the chronic drug (CD) group; 10 min activity test (Grid test inside Accuscan activity monitors).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther2	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		03				Female			20		265		164		-238		254		214		121				395		201		516		119		210		386		482		234				136		234		360		98		548		-140		428		982		261		205		466																								12/20/2002			ETSENS2(GRIDCD)		ACTD11D3	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 2 bottom	MRG 010202 with TJP from publication and data file	8627538.03
Acute Ethanol Ataxia: Grid test errors after acute 2 g/kg EtOH injection (i.p); Day 3 (first EtOH treatment) minus Day 2 (saline baseline) in the chronic drug (CD) group; 10 min test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		04				Female			114		123		135		187		86		103		143				129		154		191		165		138		227		320		289				186		108		165		132		151		185		152		298		159		164		109																								12/20/2002			ETGRID2(CD)		ERRD3D2	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 1 top	MRG 010202 with TJP from publication and data file	8627538.04
Acute Ethanol Ataxia: Grid test errors after acute 2 g/kg EtOH injection (i.p); Day 11 (only EtOH treatment) minus Day 2 (saline baseline) in the chronic saline (CS) group; 10 min test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		05				Female			116		168		150		199		91		111		201				153		140		230		210		129		195		287		351				175		110		185		106		172		256		130		337		212		171		107																								12/20/2002			ETGRID2(CS)		ERRD11D2	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 1 top inset	MRG 010202 with TJP from publication and data file	8627538.05
Change in misstep errors induced by repeated 2 g/kg EtOH injection (i.p); Day 11 (fifth EtOH treatment) minus Day 3 (first EtOH treatment) in the chronic drug (CD) group; 10 min test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		06				Female			-33		-40		33		-83		-13		-14		-18				-43		-40		64		-5		-13		-30		83		-34				-33		-10		-8		-69		-7		4		66		-63		-57		-24		47																								12/20/2002			ETGRIDTOL2(CD)		ERRD11D3	EtOH	2 g/kg	RI-82	TJP	p. 616, Fig 1 bottom	MRG 010202 with TJP from publication and data file	8627538.06
Ataxia ratio (errors/activity counts) in the Grid test after acute 2 g/kg Ethanol injection (i.p); Day 3 (first Ethanol treatment) minus Day 2 (saline baseline) in the chronic drug (CD) group; 10 min test (Grid test inside Accuscan activity monitors).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		07				Female			17.6		11.4		14.8		20.8		18.1		25.2		18.5				14.9		17.6		18		19.7		17.7		47.6		26.4		22.9				14.5		19.8		26.3		33.7		14		14.3		24.4		16.9		9		29.9		24																								12/20/2002			ETGRID2 (CD RATIO)		RATD3D2	EtOH	2 g/kg	RI-82	TJP	p. 617, Fig 3 top	MRG 010202 with TJP from publication and data file	8627538.07
Ataxia ratio (errors/activity counts) in the Grid test after acute 2 g/kg Ethanol injection (i.p); Day 11 (only EtOH treatment) minus Day 2 (saline baseline) in the chronic saline (CS) group; 10 min test (Accuscan activity Monitor Grid test).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		08				Female			15.9		14.7		14.3		19.9		26		27.5		22.7				18.2		15.1		18.1		26		17.5		47.5		24.5		24.5				16.1		17.4		27.3		27.1		17.9		18.5		22.1		17.6		11.1		32.7		22.9																								12/20/2002			ETGRID2 (CS RATIO)		RATD11D2	EtOH	2 g/kg	RI-82	TJP	p. 617, Fig 3 top inset	MRG 010202 with TJP from publication and data file	8627538.08
Change in ataxic effects of 2 g/kg Ethanol injection (i.p) after repeated treatment; Day 11 (fifth EtOH treatment) minus Day 3 (first EtOH treatment) in the chronic drug (CD) group; 10 min test (Grid test inside Accuscan activity monitors).		Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		09				Female			-6.9		-5.1		0.3		-8		-6.8		-11.2		-2.8				-8		-8.2		-1.3		-5.4		-5.3		-23.5		-0.6		-5.3				-3.8		-8.4		-10.2		-22.3		-5.8		0.8		-2.7		-8.6		-4.6		-12.4		-7.5																								12/20/2002			ETGRIDTOL2 (CD RATIO)		RATD11D3	EtOH	2 g/kg	RI-82	TJP	p. 617, Fig 3 bottom	MRG 010202 with TJP from publication and data file	8627538.09
Baseline locomotor activity measured in the grid test (photocell beam interruptions); activity on the second day (Day 2) of exposure to the testing procedure after saline injection (i.p); 10 min activity test (Accuscan Activity Monitor Grid test).	[data from all mice, regardless of subsequent treatment designation, are included in the calculation of these means.]	Ethanol (EtOH) has both locomotor stimulant and locomotor ataxic effects. Repeated EtOH treatment can result in the development of behavioral sensitization (increased sensitivity) similar to that seen with the classical stimulant drugs amphetamine and cocaine. However, it has been suggested for EtOH that sensitization may be a by-product of the development of tolerance to the sedative/ataxic effects of EtOH. It is also possible that the converse is true: that tolerance develops as the result of sensitization development. We examined this notion by measuring EtOH sensitization and tolerance in the BXD/Ty recombinant inbred strains. Changes in locomotor activation and grid test ataxia were used as the measures of sensitization and tolerance, respectively. If a genetic relationship exists between sensitization and tolerance, then those strains most susceptible to sensitization should also develop the most robust tolerance. Genetic correlations did not support the presence of this relationship. In addition, the use of the BXD/Ty recombinant inbred strains enabled us to perform gene mapping by quantitative trait locus analysis for activity and ataxia measures. We found that 28% to 79% of the genetic variation in the various activity and ataxia responses could be explained by the identified quantitative trait loci associations. However, when associations of gene markers with behavioral phenotypes were compared, we obtained no strong evidence for common genes determining magnitude of sensitization and tolerance. Thus the results of this study do not support the hypothesis that sensitization results from development of tolerance to the sedative/ataxic effects of EtOH or, conversely, that tolerance is a by-product of sensitization.	Phillips TJ, Lessov CN, Harland RD, Mitchell SR.	Evaluation of potential genetic associations between ethanol tolerance and sensitization in BXD/Ty recombinant inbred mice	J Pharmacol Exp Ther	277(2)	613-623	May	1996		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627538&dopt=Abstract	8627538		10				Female			825		877		975		795		756		873		705				641		1040		725		971		766		621		967		762				721		700		790		510		813		762		645		1596		814		693		887																								12/20/2002			SALACT(GRID10MIN)		TACTD2	Saline	0.009	RI-82	TJP	Tables 2, 3, 4, 5	MRG 010202 with TJP from publication and data file	8627538.1
Baseline locomotor activity (distance traveled); indexed as activity on the second day (Day 2) of exposure to the activity testing procedure after saline injection (ip); strain means are for a 15 min activity test (Accuscan activity monitors); data from all mice, regardless of subsequent treatment designation, are included in the calculation of these means [cm]		Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		01	52-131 days	52	131	Female	7-13	cm	2826.817	83	2799.718	112	3664.41	206	2743.583	88	2678.948	450	2617.875	125	2099.213	31	4694.203	144	1362.016	56	3449.317	111	2847.36	103	3622.441	100	3085.517	137	1983.133	159	4519.183	147	3043.587	275			2886.951	69	2093.051	147	2820.622	133	1630.075	108	2906.806	116	2545.333	147	1674.5	94	5521.39	194	3115.333	88	2654.052	127	3486.719	107																							6/4/2003	MK Sullivan		SALACT(15MIN)	BASACT	BASED2	Saline	0.9% or 10 ml/kg	RI-86	TJP	p. 3026, Fig 1 inset.	MRG 121301 by Fig 1 inset, p. 3026 Basal Activity	9526019.01
Locomotor response (distance traveled) to an acute 5 mg/kg cocaine injection (ip); indexed as Day 3 (first cocaine treatment) minus Day 2 (saline baseline) in the chronic drug (CD) group; strain means are for a 15 min activity test (Accuscan activity monitors) [cm]		Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		94	52-131 days	52	131	Female	7-13	cm	1297.667	118	2004	261	2726.25	632	2301	211	412.6	253	4.692	43	1229.417	85	3147.417	396	-468.417	0	1689.25	329	1944.4	211	2009.083	337	916.25	144	52.385	177	3776.455	674	2880.231	76			2212.25	539	745.5	0	1521.429	0	-139.818	0	1853.667	716	141.385	144	1411.231	286	571.364	505	1223.25	573	1440.364	808	317.6	640																							6/4/2003	MK Sullivan		COCACT5(CD)	ACCD5	COCAC5	Cocaine	5 mg/kg	RI-86	TJP	p. 3026, Fig 1   bottom.     	JD 121301  from file	9526019.94
Locomotor response (distance traveled) to an acute 10 mg/kg cocaine injection (ip); indexed as Day 3 (first cocaine treatment) minus Day 2 (saline baseline) in the chronic drug (CD) group; strain means are for a 15 min activity test (Accuscan activity monitors) [cm]		Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		02	52-131 days	52	131	Female	7-13	cm	2961.25	690	3386.929	782	8506.818	1261	4132.167	817	3241	652	3306.25	730	3463.417	913	5637.167	843	1755.692	817	7339	1252	3957.9	565	3418.667	548	3078.091	904	99.667	357	5716.333	791	7159.5	1261			5805.083	1122	5342.25	1504	5091.125	957	1101.545	604	4192.417	877	4569.417	1608	2988.667	609	3540.615	939	5187.231	635	4367.273	565	5093.091	1043																							6/4/2003	MK Sullivan		COCACT10(CD)	ACCD10	COCAC10	Cocaine	10 mg/kg	RI-86	TJP	p. 3026, Fig 1  top.     	JD 121301  from file	9526019.02
Locomotor response (distance traveled) to an acute 40 mg/kg cocaine injection (ip); indexed as Day 3 (first cocaine treatment) minus Day 2 (saline baseline) in the chronic drug (CD) group; strain means are for a 15 min activity test (Accuscan activity monitors) [cm]		Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		03	52-131 days	52	131	Female	7-13	cm	12932.833	758	12608.867	1238	15426.923	1592	14007.667	994	4837	733	12578.385	935	8107.417	1684	13238.75	1238	7105.692	1322	10082.538	1297	7614.1	893	8616.091	775	6817.5	1347	5307.417	1288	12385.667	935	14297.75	1625			10363.333	931	12060.889	1709	13099.286	3671	2832.9	707	7053	1263	14651.727	1120	10958.462	1625	11884.25	1213	8294.154	1811	15252.917	640	10339.917	1432																							6/4/2003	MK Sullivan		COCACT40(CD)	ACCD40	COCAC40	Cocaine	40 mg/kg	RI-86	TJP	p. 3026, Fig 1   bottom.     	JD 121301  from file	9526019.03
Cocaine induced sensitization of locomotor response (distance traveled) to 5 daily 5 mg/kg cocaine injections (i.p); Day 11 (fifth cocaine treatment) minus Day 3 (first cocaine treatment); 15 min activity test (Accuscan activity monitors) [cm]	[NOTE:  Highlighted mean was reported incorrectly in the cited publication; it is correct in this table.  All QTL analyses and genetic correlations were reported correctly in the cited publication:   'Phillips, Huson, McKinnon, 1998 JNeurosci 18: 3023-3034]	Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		93	52-131 days	52	131	Female	7-13	cm	3395.417	839	3456.857	779	3015.25	1940	1590	854	1287.444	742	1901.923	667	1616.5	419	3988.667	719	1729.25	816	1232.5	779	2971.5	382	1963.636	479	644.25	547	1597.231	577	630.455	903	3115.231	188			1851.833	921	1931.125	1258	3096.714	816	1753.182	442	2246.25	861	4200.308	995	3825.538	1131	1217.455	841	3591.333	839	1692.818	712	4256.778	779																							6/4/2003	MK Sullivan		COCSEN5(CD)	deltaCD5	COCSEN5	Cocaine	5 mg/kg	RI-86	TJP	p.3027, Fig 2	JD 121301  from publication	9526019.93
Cocaine induced sensitization of locomotor response (distance traveled) to 5 daily 10 mg/kg cocaine injections(ip); indexed as Day 11 (fifth cocaine treatment) minus Day 3 (first cocaine treatment); 15 min activity test (Accuscan activity monitors) [cm]		Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		04	52-131 days	52	131	Female	7-13	cm	3823	839	4570.714	644	6091.364	2548	2503.727	1030	3704.727	1184	6180	951	2812.917	1487	4479.333	1294	1517.231	1040	1760.833	1110	4708	925	3883.5	782	3864.5	1026	893.083	419	3789	921	8423.75	653			5866.083	1041	4600	2382	2285.5	1086	2925.818	404	4008.583	1491	5286.583	2494	4198.75	1139	-1518.923	1108	2158	1169	3725.273	813	4234.818	1063																							6/4/2003	MK Sullivan		COCSEN10(CD)	deltaCD10	COCSEN10	Cocaine	10 mg/kg	RI-86	TJP	p.3027, Fig 2	JD 121301  from publication	9526019.04
Cocaine induced sensitization of locomotor response (distance traveled) to 5 daily 40 mg/kg cocaine injections (ip); indexed as Day 11 (fifth cocaine treatment) minus Day 3 (first cocaine treatment) distance traveled (in cm);  15 min activity test (Accuscan activity monitors) [cm]	 	Sensitization to the psychostimulant effects of cocaine has received widespread attention because concomitant changes occur in neurochemical pathways that are part of the brain reward pathway. The current study was undertaken with the purpose of mapping genes determining sensitivity to the acute stimulant and sensitizing effects of cocaine. Sensitivity and sensitization to cocaine (5, 10, and 40 mg/kg) were measured in 25 BXD/Ty recombinant inbred (BXD RI) strains and the progenitor C57BL/6J (B6) and DBA/2J (D2) strains. Quantitative trait locus (QTL) mapping provisionally localized cocaine sensitivity genes to regions on all chromosomes except 6, 11, 17, and X; sensitization QTLs were localized to chromosomes 1-10, 13, 15, 18, 19, and X. Provisional QTLs for locomotion after saline injection in a novel setting were mapped to chromosomes 1, 3-6, 9, 12, 13, 18, and 19 and in a familiar setting to chromosomes 4-7, 9, 13, and 19. There were both common and unique QTL regions across the phenotypes. Evidence for a genetic association between magnitude of acute cocaine response and sensitization was obtained for only the 10 mg/kg dose. Some common QTL regions for cocaine, ethanol, and methamphetamine responses suggest the possibility that these drugs induce stimulant effects or sensitization through some common mechanisms. However, independent mechanisms were also indicated. Many candidate genes reside near the provisional QTLs mapped for cocaine responses, including genes coding a variety of neurotransmitter and hormone receptors. These data, once confirmed, should prove useful for directing investigations of acute and chronic cocaine effects down already suspected and novel avenues.	Phillips TJ, Huson MG, McKinnon CS.	Localization of genes mediating acute and sensitized locomotor responses to cocaine in BXD/Ty recombinant inbred mice	J Neurosci 	18(8)	3023-3034	Apr	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526019&dopt=Abstract	9526019		05	52-131 days	52	131	Female	7-13	cm	-1069.333	1367	1470.4	1709	5966.538	2300	-2287.75	1441	4268.083	1252	1017.154	1108	3505.167	1929	2721.333	2071	872.615	1940	-4245.615	1650	7010.8	1476	993.364	1175	471.5	2017	3670.333	2127	3281.25	1976	5300.333	2182			3580.833	1086	-2874.444	2408	2053.143	5161	4624.7	1236	-2123.308	1700	-3130.7	1805	2830.692	1536	-283.833	1124	4110.538	2840	2393.417	1022	3420.25	2060																							6/4/2003	MK Sullivan		COCSEN40(CD)	deltaCD40	COCSEN40	Cocaine	40 mg/kg	RI-86	TJP	p.3027, Fig 2	JD 121301  from publication	9526019.05
Locomotor response (distance traveled in cm) to 20% 2-hydroxypropyl-beta-cyclodextrin vehicle injection (ip); indexed as Day 3 (third vehicle treatment) minus Day 2 (vehicle baseline) in the vehicle control group; strain means are for a 30 min activity test (Accuscan activity monitors).		Allopregnanolone is a neuroactive steroid that, like ethanol (EtOH), has stimulant, anxiolytic, ataxic, and depressant effects. Two experiments tested the hypothesis that sensitivity to the locomotor stimulant effects of these drugs is influenced by a common set of genes. Sensitivity to the locomotor stimulant effects of allopregnanolone was determined in 24 BXD recombinant inbred (RI) strains. Strain means were positively correlated with extant means for EtOH stimulation in 20 of the same strains. Quantitative trait locus (QTL) analysis provisionally identified many loci, including several known to influence sensitivity to EtOH. Sensitivity to allopregnanolone was also measured in FAST and SLOW mice, which were selectively bred for differential locomotor response to EtOH, to determine whether selection has also altered allopregnanolone sensitivity. FAST mice were more sensitive to the stimulant effects of allopregnanolone compared with SLOW mice. These data suggest that sensitivity to the locomotor stimulant effects of these drugs is influenced by common genes.	Palmer AA, Miller MN, McKinnon CS, Phillips TJ	Sensitivity to the locomotor stimulant effects of ethanol and allopregnanolone is influenced by common genes	Behav Neurosci 	116(1)	126-137	Feb	2002 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11895174&dopt=Abstract	11895174		01	50-123 days	50	123	Female	10-27	cm	-88.04762268	479.78	-640.5999756	319.13	-321.125	416.39	-1170.300049	159.02	-1008.166687	412.57	-1589.119995	461.75	-174.1538391	278.69	-816	798.09	-483.9285583	300.01	-923.833313	274.59	-25.81818199	366.12	-1479.083374	300.02	-1180.153809	805.46	-207.9166718	551.37	-535.6153564	560.38	276.0666809	327.32			-408.7692261	456.56	-408.6923218	284.70			-204.5	415.85	-1464.230713	289.62	285.2142944	356.56	-521.4615479	260.11	-1958.199951	566.12	-312.615387	294.54	-524.4615479	258.20	-620.2272949	358.47																							6/23/2003	MK Sullivan		VEHACT(30MIN)		ALLO-0	Allopregnanolone	0mg/kg	RI-163	TJP/AAP	p.129, Fig 1	MRG and AAP 02/06/02	11895174.01
Locomotor response (distance traveled in cm) to 10 mg/kg allopregnanolone (3a-hydroxy-5a-pregnan-20-one, THP) in 20% 2-hydroxypropyl-beta-cyclodextrin vehicle injection (ip); indexed as Day 3 (first allopregnanolone treatment) minus Day 2 (vehicle baseline); strain means are for a 30 min activity test (Accuscan activity monitors).		Allopregnanolone is a neuroactive steroid that, like ethanol (EtOH), has stimulant, anxiolytic, ataxic, and depressant effects. Two experiments tested the hypothesis that sensitivity to the locomotor stimulant effects of these drugs is influenced by a common set of genes. Sensitivity to the locomotor stimulant effects of allopregnanolone was determined in 24 BXD recombinant inbred (RI) strains. Strain means were positively correlated with extant means for EtOH stimulation in 20 of the same strains. Quantitative trait locus (QTL) analysis provisionally identified many loci, including several known to influence sensitivity to EtOH. Sensitivity to allopregnanolone was also measured in FAST and SLOW mice, which were selectively bred for differential locomotor response to EtOH, to determine whether selection has also altered allopregnanolone sensitivity. FAST mice were more sensitive to the stimulant effects of allopregnanolone compared with SLOW mice. These data suggest that sensitivity to the locomotor stimulant effects of these drugs is influenced by common genes.	Palmer AA, Miller MN, McKinnon CS, Phillips TJ	Sensitivity to the locomotor stimulant effects of ethanol and allopregnanolone is influenced by common genes	Behav Neurosci 	116(1)	126-137	Feb	2002 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11895174&dopt=Abstract	11895174		02	50-123 days	50	123	Female	10-27	cm	3477.600098	805.79	3019.899902	519.83	598.4666748	781.82	2017.666626	730.58	846.3076782	785.08	1093.136353	445.45	1020	379.34	1203.588257	1160.33	674	549.59	1166.058838	702.48	1419.272705	495.45	1484.75	644.63	1831.769287	645.04	3109.764648	1121.90	1081.692261	533.88	2940.642822	752.89			994.916687	772.31	1652.583374	479.34			337.0909119	523.97	523.6923218	582.64	801.7142944	353.72	1036.230713	379.34	1559	873.97	11	398.76	393.6666565	355.79	694.458313	534.30																							6/23/2003	MK Sullivan		ALLOACT10		ALLO-10	Allopregnanolone	10mg/kg	RI-163	TJP/AAP	p.129, Fig 1	MRG and AAP 02/06/02	11895174.02
Locomotor response (distance traveled in cm) to 17 mg/kg allopregnanolone (3a-hydroxy-5a-pregnan-20-one) in 20% 2-hydroxypropyl-beta-cyclodextrin vehicle injection (ip); indexed as Day 3 (first allopregnanolone treatment) minus Day 2 (vehicle baseline); strain means are for a 30 min activity test (Accuscan activity monitors).		Allopregnanolone is a neuroactive steroid that, like ethanol (EtOH), has stimulant, anxiolytic, ataxic, and depressant effects. Two experiments tested the hypothesis that sensitivity to the locomotor stimulant effects of these drugs is influenced by a common set of genes. Sensitivity to the locomotor stimulant effects of allopregnanolone was determined in 24 BXD recombinant inbred (RI) strains. Strain means were positively correlated with extant means for EtOH stimulation in 20 of the same strains. Quantitative trait locus (QTL) analysis provisionally identified many loci, including several known to influence sensitivity to EtOH. Sensitivity to allopregnanolone was also measured in FAST and SLOW mice, which were selectively bred for differential locomotor response to EtOH, to determine whether selection has also altered allopregnanolone sensitivity. FAST mice were more sensitive to the stimulant effects of allopregnanolone compared with SLOW mice. These data suggest that sensitivity to the locomotor stimulant effects of these drugs is influenced by common genes.	Palmer AA, Miller MN, McKinnon CS, Phillips TJ	Sensitivity to the locomotor stimulant effects of ethanol and allopregnanolone is influenced by common genes	Behav Neurosci 	116(1)	126-137	Feb	2002 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11895174&dopt=Abstract	11895174		03	50-123 days	50	123	Female	10-27	cm	2414.730703	681.74	5722.411621	908.71	2639.666748	1427.39	4524.90918	1020.75	2317.923096	732.37	3171.173828	763.49	3867.769287	945.64	3759.9375	1386.72	4051	1248.13	3099.882324	598.34	2904.916748	900.03	2294.166748	924.90	3454.230713	743.57	4645.222168	1361.00	5758.307617	1327.80	5285.5	1641.08			4636.692383	1079.67	3529.083252	788.38			3781	1045.64	4282.143066	1526.97	6489.571289	1573.44	428.1666565	542.74	5010.5	1568.46	6124.307617	1369.71	2913.083252	968.46	4020.407471	622.41																							6/23/2003	MK Sullivan		ALLOACT17		ALLO-17	Allopregnanolone	17mg/kg	RI-163	TJP/AAP	p.129, Fig 1	MRG and AAP 02/06/02	11895174.03
Ethanol acceptance - Ratio relative to water (within mouse)	Alcohol Acceptance Ratio; ratio of ethanol intake (ml) on test day to average water intake (ml) measured on first two days	Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		01				Male			0.75		0.29		0.44				1.09		0.07		0.53				0.67		0.67				0.34		0.49		0.73				0.66				0.5				0.82		0.44		0.08				0.04		0.63		0.18																												12/20/2002			ETACC10	ACCRATIO	ACCRATIO	EtOH	10% EtOH		JCC	p. 184, Table 2	JD 020502  from publication	6683363.01
Ethanol acceptance - Total ethanol intake [g/kg]		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		02				Male			12.6		3.36		3.52				9.95		1.32		10.89				13.34		8.9				8.29		7.65		9.34				10.21				12.66				10.78		2.43		1.03				0.68		4.81		2.34																												12/20/2002			ETCONS10	ETINTAKE	ETINTAKE	EtOH	10% EtOH    ( v/v)		JCC	p. 184, Table 2	MRG 120601 from publication	6683363.02
Saline open Field Activity - beam interruptions after saline administration		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		03				Male			155		132		175		182		240		152		113				79		141		127		152		104		158		131		166				171				159		125				134		89		171		95																												12/20/2002			SALACT	OFA	OFACTIV	Saline			JCC	p. 184, Table 1	MRG 120601 from publication	6683363.03
Ethanol open field activity - beam interruptions after EtOH administration		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		04				Male			83		335		264		155		178		144		171				133		317		121		245		117		252		150		268				251				204		154				187		170		226		233																												12/20/2002			ACT1.3	ETOFA	ETACTIV	EtOH	1.33 g/kg		JCC	p. 184, Table 1	JD 020502  from publication	6683363.04
Ethanol open field activity - difference relative to saline	EtOH Effect on Open field activity. Activity (beam interruptions) in 4 min (day 2 - day 1) or (ETOFA - OFA)	Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		05				Male			-72		203		89		-27		-62		-8		58				54		176		-6		93		13		94		19		102				80				45		29				53		81		55		138																												12/20/2002			ETACT1.33(delta)	ACT	ETDELTOF	EtOH	1.33 g/kg		JCC	p. 184, Table 1	MRG 120601 from publication	6683363.05
Ethanol induced ataxia, Errors/run on grid test, 2 min - 10 min post-EtOH injection		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		06				Male			2.58		1.84		1.66		2.4				2.28		5.43																		3.18										2.25						1.84				2.5																												12/20/2002			ETGRID2.5	GT	ETGRID	EtOH	2.5 g/kg		JCC	p. 185, Table 3	MRG 120601 from publication	6683363.06
Chronic ethanol withdrawal - handling induced convulsion,  1.5 g/kg loading dose and 68.1mg/kg pyrazole; 15 hr area under curve		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		07				Male			14.5		29				34.5										23.75		21.13				22.83		16										7.5										32.5						25.33																												12/26/2002			ETHIC(VAP)	WDR	AREA	EtOH	Varied vapor conc	Exp1	JCC	p. 185, Table 4	MRG 021502 from publication	6683363.07
Chronic ethanol withdrawal - handling induced convulsion,  1.5 g/kg loading dose and 68.1mg/kg pyrazole; 15 hr area under curve		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		08				Male							28.3		29.83				11.83						41.3						25.88		11.75														15		28.17				35.3				5																														12/20/2002			ETHIC(VAP)	WDR	AREA	EtOH	Varied vapor conc	Exp2	JCC	p. 185, Table 4	MRG 021502 from publication	6683363.08
Chronic ethanol withdrawal - handling induced convulsion,  1.5 g/kg loading dose and 68.1mg/kg pyrazole; 15 hr area under curve		Male mice of parent inbred strains C57BL/6J and DBA/2J, and mice from several of the BXD/Ty Recombinant Inbred (RI) strains derived from the cross of the parent inbred strains were tested for responsiveness to ethanol. Separate groups of mice from these strains were characterized for sensitivity to ethanol's effects to increase activity in an open field and to induce ambulatory ataxia in the grid test. The strain distribution pattern of the RI strains indicated polygenic control of both responses to ethanol. Other mice from this battery were tested for acceptance of an ethanol solution, a measure related to preference drinking. This trait may be substantially influenced by a single gene. Mice were then rendered physically dependent on ethanol through inhalation of ethanol vapor for three days. Severity of handling-induced convulsions was used to index the severity of the ethanol withdrawal syndrome. The distribution of the RI strains indicated possible influence of a major gene on ethanol withdrawal severity.	Crabbe JC, Kosobud A, Young ER, Janowsky JS.	Polygenic and single-gene determination of responses to ethanol in BXD/Ty recombinant inbred mouse strains	Neurobehav Toxicol Teratol	5(2)	181-187	Mar-Apr	1983 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6683363&dopt=Abstract	6683363		09				Male			11.83		28		19.43						13.64																		8												22.75				7.5		9.83		4		23.67																												12/20/2002			ETHIC(VAP)	WDR	AREA	EtOH	Varied vapor conc	Exp3	JCC	p. 185, Table 4	MRG 021502 from publication	6683363.09
Ethanol hypothermic sensitivity 2 g/kg [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.                                2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	184-192	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		92				Female		degree C	-2		-1.628		-1.153		-1.344		-2.374		-2.255		-1.231		-2.642		-0.594		-1.27		-1.296		-1.617		-0.875		-0.853		-1.439		-1.038				-1.394		-1.631				-1.328		-1.861		-0.877		-1.096		-1.908		-0.602				-1.492																								12/26/2002			ETTEMP2	HT2	AVED1E2	EtOH	2 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.92
Ethanol hypothermic sensitivity 3 g/kg [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.                                2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	624-632    	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		91				Female		degree C	-3.1		-1.601		-2.083		-2.467		-3.174		-2.904		-1.797		-3.331		-1.008		-2.921		-2.583		-1.733		-2.528		-1.909		-2.225		-2.654				-1.793		-3.167				-1.856		-2.386		-3.146		-2.192		-2.449		-1.595				-2.363																								12/26/2002			ETTEMP3	HT3	AVED1E3	EtOH	3 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.91
Ethanol hypothermic sensitivity 4 g/kg [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.                                2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	624-632    	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		90				Female		degree C	-3.96		-2.934		-2.233		-2.528		-3.651		-3.479		-2.109		-3.467		-1.514		-2.979		-3.73		-3.9		-3.323		-1.826		-2.71		-2.549				-2.742		-2.769				-2.403		-2.067		-4.285		-2.312		-2.922		-2.101				-3.086																								12/26/2002			ETTEMP4	HT4	AVED1E4	EtOH	4 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.9
Hypothermia tolerance (positive scores) or sensitization(negative scores) 2 g/kg ethanol, day 3 - day 1 [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.   2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	624-632    	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		89				Female		degree C	-0.495		-0.564		-0.014		-0.225		-0.035		-0.692		-0.103		-0.408		-0.008		-2.17		-0.252		-0.597		-0.019		0.053		0.189		-0.153				-0.066		0.503				0.161		-0.295		0.108		0.424		-0.752		-0.019				-0.444																								12/26/2002			ETTEMPTOL2	TOL2	DDAV13E2	EtOH	2 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.89
Hypothermia tolerance (positive scores) or sensitization(negative scores) 3 g/kg ethanol, day 3 - day 1 [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.                                2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	624-632    	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		88				Female		degree C	-0.907		0.058		-0.316		-0.569		0.023		-0.439		-0.181		-0.687		0.003		-0.697		-0.164		0.1		-0.991		-0.338		-0.366		-0.759				0.727		-0.178				1.122		-0.505		-0.492		-5.13		-0.179		-0.464				-0.229																								12/26/2002			ETTEMPTOL3	TOL3	DDAV13E3	EtOH	3 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.88
Hypothermia tolerance (positive scores) or sensitization(negative scores) 4 g/kg ethanol, day 3 - day 1 [degrees C]	[1)  Initial report given in Crabbe, Belknap, Mitchell, Crawshaw, 1994 JPET 269:184-192.                                2)  QTL analyses performed as described in Crabbe, Phillips, Gallaher, Crawshaw, Mitchell, 1996 JPET 277: 624-632              3)  For the '96 paper, data for additional strains were added and some additional mice.  Complete data set for the '96 paper is presented here in this database]	Sensitivity and tolerance to ethanol-induced ataxia and hypothermia are determined in part by genetic factors; some genes that affect one of these traits may affect others as well. To test this general hypothesis, we examined hypothermia and two tests of ataxia in the C57BL/6J and DBA/2J inbred mouse stains and in 18 to 25 of their recombinant inbred strains. Genetic correlations among strain mean responses revealed strong positive associations of genetic origin between sensitivity and tolerance for each of the three responses. Furthermore, tolerance to grid test ataxia and tolerance to hypothermia were positively associated. Sensitivity scores across the three responses were uncorrelated. The second method employed to assess genetic correlation was to examine the pattern of genetic locations of quantitative trait loci (QTLs) provisionally identified using genetic mapping procedures. This method identified 3 to 14 QTLs associated with each trait. Within each response, a number of these associations were in common for measures of sensitivity and tolerance; this suggests the existence of several specific genes that exert pleiotropic effects on sensitivity and tolerance. In a result consistent with the analyses of genetic correlations, there was modest evidence for QTLs associated across measures. Some QTLs associated with multiple traits mapped to chromosomal regions where candidate genes (e.g., genes for neurotransmitter receptors) have been mapped. In summary, the analyses presented suggest modest commonality of genetic influence on tolerance to some measures of ataxia and hypothermia, and they strongly support previous data indicating that sensitivity and tolerance to specific effects of ethanol share common genetic determinants.	Crabbe JC, Phillips TJ, Gallaher EJ, Crawshaw LI, Mitchell SR.	Common genetic determinants of the ataxic and hypothermic effects of ethanol in BXD/Ty recombinant inbred mice: genetic correlations and quantitative trait loci.	J Pharmacol Exp Ther	277(2)	624-632    	May	1996 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627539&dopt=Abstract	8627539 		87				Female		degree C	-0.78		-0.922		0.097		-0.354		-0.679		-0.863		0.136		-0.025		-0.356		-0.363		-0.667		-1.278		-1.139		0.108		-0.465		-0.559				-0.5		-0.343				0.444		-0.6		0.722		-0.573		-0.381		-1.031				-0.972																								12/26/2002			ETTEMPTOL4	TOL4	DDAV13E4	EtOH	4 g/kg	RI-50	JCC		JRS 2/11/00 from data file	8627539.87
Baseline Temp (C) for Day 1 before Quinpirole injection 		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet  	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		01	10-14 wks	70	98	Female			38.711		38.687				38.851		38.724		38.69		39.37		38.721		39.227		38.958		38.581		38.645		38.565		38.369		38.192		38.247				39.009		39.074		38.79		38.453		39.183		38.67		38.7		39.449		38.46		38.168		39.068																								12/20/2002			NULTEMP	BASET	BASECD1	Quinpirole	1mg/kg	RI-69	JCC		JD 121901  from data file	11054779.01
Hypothermia measured 60 min after quinpirole administration on day 1; change from baseline temperature [degrees C] 		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		02	10-14 wks	70	98	Female		degrees C	-1.622	0.200	-5.043	0.243			-3.847	0.296	-1.144	0.210	-3.634	0.252	-4.746	0.390	-4.374	0.343	-1.224	0.157	-2.074	0.152	-0.874	0.233	-2.673	0.204	-1.127	0.091	-2.798	0.273	-1.573	0.314	-6.465	0.324			-3.295	0.272	-1.781	0.181	-3.488	0.309	-2.557	0.168	-2.4	0.271	-3.615	0.305	-6.767	0.590	-2.089	0.195	-3.831	0.315	-1.115	0.117	-3.967	0.258																							7/1/2003	MK Sullivan		QPTEMP1	HT60	DEL60D1	Quinpirole	1mg/kg	RI-69	JCC	p. 700, Fig 2a	JD 121901  from data file	11054779.02
Tolerance to quinpirole induced hypothermia on day 2 as compared to day 1 [degrees C]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		03	10-14 wks	70	98	Female		degrees C	-0.242		-0.735				-0.918		-0.18		-1.153		-1.407		-1.184		-0.34		-0.056		-0.202		-0.386		0.03		-0.768		-0.636		-2.019				-0.754		-0.542		-1.215		-0.457		-0.692		-0.688		-2.167		-0.461		-1.024		-0.226		-1.718																											QPTEMPTOL1(D2)	HT TOL2	TOL60D12	Quinpirole	1mg/kg	RI-69	JCC		JD 121901  from data file	11054779.03
Tolerance to quinpirole induced hypothermia on day 3 as compared to day 1 [degrees (C)]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		04	10-14 wks	70	98	Female		degrees C	-0.758	0.158	-1.652	0.262			-1.472	0.214	-0.262	0.177	-2.213	0.205	-2.151	0.328	-1.412	0.295	-0.636	0.214	-0.234	0.159	-0.139	0.162	-0.978	0.199	-0.296	0.150	-1.374	0.270	-1.015	0.214	-3.181	0.402			-1.102	0.266	-0.936	0.193	-1.321	0.208	-1.038	0.167	-0.575	0.243	-0.528	0.281	-2.867	0.476	-1.222	0.178	-0.569	0.210	-0.390	0.121	-2.197	0.223																							7/2/2003	MK Sullivan		QPTEMPTOL1(D3)	HT TOL3	TOL60D13	Quinpirole	1mg/kg	RI-69	JCC	p. 700, Fig 2b	JD 121901  from data file	11054779.04
Activity after saline administration (baseline); distance traveled [cm]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet  	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		05	10-14 wks	70	98	Female	10-44	cm	4856.45	294.2	3130	174.3			3465.56	133.6	2872.5	20.3	4197.17	309.1	3103.19	197.1	3973.81	124.9	1348.96	157.7	4790.5	236.5	2741.05	256.0	4112.67	231.5	4431	334.0	2289.59	150.2	4913.86	286.7	3254.37	190.9			3430.68	223.7	2475.78	136.9	2849.41	155.6	1952.25	83.8	4462.47	345.2	2008.57	158.5	2237.4	128.6	6160.66	266.4	3338.65	144.8	3182.64	161.4	4400.74	207.5																							7/1/2003	MK Sullivan		SALACT	ACT BASAL	STHDIST	Saline		RI-69	JCC	p. 699, Fig 1a	JD 121901  from data file	11054779.05
Activity decrease after administration of 0.01 mg/kg  quinpirole; difference from basal activity, distance traveled [cm] 		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		06	10-14 wks	70	98	Female	10-44	cm	-2878.27	407.2	-843.33	202.3			-1327.56	190.2	-1165.64	136.6	-2840.87	341.5	-1098.64	262.6	-1016.06	152.1	-735.08	241.8	-3267.53	356.7	-1597.27	427.6	-956.22	319.3	-1714.36	586.3	-999.5	213.4	-2063.09	260.1	-1038.57	178.4			-1214.11	260.8	-1095.88	164.9	-902.82	251.3	-848.6	108.2	-1845.5	309.3	-459.14	196.4	-786.2q	228.9	-2773.6	301.0	-914.67	238.1	-1319.57	193.0	-1696.27	277.8																							7/1/2003	MK Sullivan		QPACT.01(delta)	ACT DECR01	DELHD01	Quinpirole	.01 mg/kg	RI-69	JCC		JD 121901  from data file	11054779.06
Activity decrease after administration of 0.03 mg/kg  quinpirole; difference from basal activity, distance traveled [cm]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		07	10-14 wks	70	98	Female			-2963.64		-1541.71				-1777.94		-1658.43		-2678.6		-1934.9		-1839.38		-808.92		-3388.47		-1582		-2256.11		-2761.92		-1368.38		-2667.27		-2029.77				-1945.8		-1501.44		-1162.07		-1158.05		-1969.09		-717.06		-1669.6		-3768.1		-1573.64		-1691.86		-2403.35																								12/20/2002			QPACT.03(delta)	ACT DECR03	DELHD03	Quinpirole	.03 mg/kg	RI-69	JCC	p. 699, Fig 1b	JD 121901  from data file	11054779.07
Rearing after saline administration [number of beam interruptions]	[Unpublished means from same series of studies as reported in:     Buck, Lischka, Dorow, Crabbe, 2000  AmerJMedGenet (NeuropsychiGenet) 96:696-705]	Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		86	10-14 wks	70	98	Female		number of beam interruptions	277.448		356.462				173.882		167.357		263.933		330.952		357.313		114.48		273		195.545		214.556		220.783		184.235		249.455		272.741				296.737		99.813		214.813		84.85		299.158		118.467		136.8		282		335.217		210.048		380.095																								12/19/2002			SALREAR	REAR BASAL	STVACT	Saline		RI-69	JCC		JD 121901  from file	11054779.86
Rearing decrease after 0.01 mg/kg quinpirole; difference from basal rearing, [number of beam interruptions]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet  	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		85	10-14 wks	70	98	Female			-124.267		-77.33				-27.375		-57.286		-164.4		-101.636		-86.125		-54.615		-150.53		-105.091		-23.333		-52.182		-64		-20.364		-88.571				-62.667		-31.875		-72.706		-33.1		-126.25		9.571		-32		-102.1		-49.5		-55.333		-153.273																								12/19/2002			QPREAR.01(delta)	REAR DECR01	DELVAC01	Quinpirole	.01 mg/kg	RI-69	JCC		JD 121901  from file	11054779.85
Rearing decrease after 0.03 mg/kg quinpirole; difference from basal rearing, [number of beam interruptions]		Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.	Buck K, Lischka T, Dorow J, Crabbe J.	Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors	Amer J Med Genet 	96(5)	696-705	Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11054779&dopt=Abstract	11054779		84	10-14 wks	70	98	Female			-184.5		-180.286						-66.56		-79.571		-137.2		-168.2		-120.875		-74.833		-201.2		-104.545		-120.333		-120.167		-115.38		-83.273				-148.308		-179.4		-77.625		-78.267		-29.1		-162.909		-20.25		-89.2		-123.714		-157.27		-107.714																						-216.857		12/19/2002			QPREAR.03(delta)	REAR DECR03	DELVAC03	Quinpirole	.03 mg/kg	RI-69	JCC		JD 121901  from file	11054779.84
BEC (blood ethanol concentration) from the retro-orbital sinus at recovery of righting reflex [mg/ml]		BACKGROUND: Genetic and environmental factors contribute to an individual's sensitivity to ethanol, although the exact genes underlying ethanol's effects are not known. Quantitative trait locus (QTL) mapping is one successful method for provisionally identifying genes participating in the mediation of a given behavior. QTL analyses seek to identify associations between a quantitative response and previously mapped marker genes across genetically diverse individuals. Many QTL analyses have been performed in BXD recombinant inbred (RI) strains of mice derived from a cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. METHODS: We conducted a QTL analysis of ethanol-induced loss of righting reflex and ataxia using a panel of 25 BXD RI strains and the progenitors B6 and D2. We measured the duration of loss of righting reflex after injection and blood ethanol concentrations upon regaining of righting reflex. Ataxia was measured as the latency to fall from a vertical screen. RESULTS: Genome-wide QTL analyses correlating strain means with allelic status at >1500 markers identified several associations (p < or = 0.01). These provisional QTLs were on all chromosomes except 2, 5, 12, 13, and X, and several map near potential candidate genes. CONCLUSIONS: These results suggest that ethanol sensitivity is determined by the actions of multiple genes and further suggest their general chromosomal map locations. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Browman KE, Crabbe JC.	Quantitative trait loci affecting ethanol sensitivity in BXD recombinant inbred mice	Alcohol Clin Exp Res	24(1)	17-23	Jan	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10656187&dopt=Abstract	10656187		01	8-18 wks	56	126	Female	4-18	mg/ml	3.915	0.231	3.58	0.098	3.788	0.070	3.46	0.087	3.966	0.104	3.453	0.079	3.971	0.101			3.894	0.100	3.406	0.114	3.837	0.048	3.846	0.078	3.899	0.178	3.446	0.078	3.547	0.124	3.266	0.128			3.581	0.125	3.406	0.099	4.084	0.136	3.813	0.106	3.651	0.073	4.121	0.162	4.002	0.084	3.757	0.109	4.129	0.155	3.634	0.073	3.843	0.140																							7/16/2003	MK Sullivan		ETLORRBEC4.1	LRRBEC	BEC            LORR	EtOH	4.1 g/kg     20% V/V 	RI-80	JCC	p.19, Fig 1A	JRS 2/11/00 and JD with JCC 020702	10656187.01
Duration of post-ethanol loss of righting reflex [minutes]		BACKGROUND: Genetic and environmental factors contribute to an individual's sensitivity to ethanol, although the exact genes underlying ethanol's effects are not known. Quantitative trait locus (QTL) mapping is one successful method for provisionally identifying genes participating in the mediation of a given behavior. QTL analyses seek to identify associations between a quantitative response and previously mapped marker genes across genetically diverse individuals. Many QTL analyses have been performed in BXD recombinant inbred (RI) strains of mice derived from a cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. METHODS: We conducted a QTL analysis of ethanol-induced loss of righting reflex and ataxia using a panel of 25 BXD RI strains and the progenitors B6 and D2. We measured the duration of loss of righting reflex after injection and blood ethanol concentrations upon regaining of righting reflex. Ataxia was measured as the latency to fall from a vertical screen. RESULTS: Genome-wide QTL analyses correlating strain means with allelic status at >1500 markers identified several associations (p < or = 0.01). These provisional QTLs were on all chromosomes except 2, 5, 12, 13, and X, and several map near potential candidate genes. CONCLUSIONS: These results suggest that ethanol sensitivity is determined by the actions of multiple genes and further suggest their general chromosomal map locations. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Browman KE, Crabbe JC. 	Quantitative trait loci affecting ethanol sensitivity in BXD recombinant inbred mice	Alcohol Clin Exp Res	24(1)	17-23	Jan	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10656187&dopt=Abstract	10656187		02	8-18 wks	56	126	Female	4-18	minutes	88.222	9.55	87.254	7.01	130.45	15.74	172.442	10.07	114.3	21.78	131.204	18.04	93.668	10.82			82.472	8.71	176.828	10.60	148.655	22.79	94.72	7.75	122.329	7.75	124.98	24.83	182.56	21.34	194.169	28.89			132.467	16.44	155.08	27.73	111.9	15.81	138.067	8.02	113.967	6.26	161.538	35.27	118.362	13.22	122.59	10.07	56.071	5.07	124.086	8.59	178.463	21.01																							7/16/2003	MK Sullivan		ETLORR4.1	LRRDUR	DURATION   LORR	EtOH	4.1 g/kg     20% V/V 	RI-80	JCC	p.19, Fig 1B	JRS 2/11/00 and JD with JCC 020702	10656187.02
Ethanol induced ataxia - Screen test sensitivity, latency to fall, saline response minus 2.5 g/kg Ethanol response [seconds] 	[NOTE: dose was reported incorrectly in the cited publication]	BACKGROUND: Genetic and environmental factors contribute to an individual's sensitivity to ethanol, although the exact genes underlying ethanol's effects are not known. Quantitative trait locus (QTL) mapping is one successful method for provisionally identifying genes participating in the mediation of a given behavior. QTL analyses seek to identify associations between a quantitative response and previously mapped marker genes across genetically diverse individuals. Many QTL analyses have been performed in BXD recombinant inbred (RI) strains of mice derived from a cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. METHODS: We conducted a QTL analysis of ethanol-induced loss of righting reflex and ataxia using a panel of 25 BXD RI strains and the progenitors B6 and D2. We measured the duration of loss of righting reflex after injection and blood ethanol concentrations upon regaining of righting reflex. Ataxia was measured as the latency to fall from a vertical screen. RESULTS: Genome-wide QTL analyses correlating strain means with allelic status at >1500 markers identified several associations (p < or = 0.01). These provisional QTLs were on all chromosomes except 2, 5, 12, 13, and X, and several map near potential candidate genes. CONCLUSIONS: These results suggest that ethanol sensitivity is determined by the actions of multiple genes and further suggest their general chromosomal map locations. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Browman KE, Crabbe JC. 	Quantitative trait loci affecting ethanol sensitivity in BXD recombinant inbred mice	Alcohol Clin Exp Res	24(1)	17-23	Jan	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10656187&dopt=Abstract	10656187		03	7-20	49	140	Female	4-18	seconds	45.155	3.30	16.107	6.19	43.169	4.02	43.434	0.04	27.264	11.30	33.383	6.15	42.943	4.77	35.512	8.25	16.804	7.27	41.471	1.99	36.536	6.04	36.324	5.05	36.524	6.26	46.496	4.28	40.204	4.76	30.813	7.18			35.676	5.87	27.141	7.75	25.203	13.78	21.797	6.97	32.526	6.79	28.99	8.60	39.616	7.68	49.821	1.21	24.452	8.69	46.511	5.34	40.265	3.61																							7/16/2003	MK Sullivan		ETSCR2(delta)	SCREEN	DELLAT        SCREEN	EtOH	2.5g/kg	RI-80	JCC	p.19, Fig 1C	JRS 2/11/00 and JD with JCC 020702	10656187.03
Area under the 25-hr curve for withdrawal following 72 hr exposure to EtOH vapor. Pyrazole injections were given daily to inhibit EtOH metabolism. Handling-induced convulsions (HIC) were scored hourly for 10 hr and again at hrs 24 and 25 [seizure severity]		Male mice from C57BL/6J (B6), DBA/2J (D2) and their 25 recombinant inbred (RI) strains were exposed to ethanol (EtOH) vapor (3.0-9.0 mg EtOH/liter of air) for 72 hr. Mice were selected such that each strain averaged 1.34 to 1.59 mg of EtOH/ml of blood on withdrawal. Control groups and EtOH-exposed groups were tested hourly for handling-induced convulsions (HIC) for 10 hr and at hr 24 and 25. Strain withdrawal severity was indexed as the area under the 25-hr HIC curve for the EtOH group minus that strain's equivalent value for the control group. Genome-wide quantitative trait locus (QTL) analyses correlating strain means with allelic status at > 1500 markers identified 10 chromosomal regions at P < .01. These provisionally identified QTLs were on chromosomes 1 (2 QTLs), 3, 9 (2 QTLs), 10, 12, 13, 15 and 18. Multiple regression analysis using the four most influential QTLs revealed that these loci controlled 86% of the genetic variance. A QTL mapped to distal chromosome 1 (P < .001) is in the same region as one previously definitively mapped for acute alcohol withdrawal, as well as one mapped for acute pentobarbital withdrawal. Several of the QTLs map near potential candidate genes. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Crabbe JC 	Provisional mapping of quantitative trait loci for chronic ethanol withdrawal severity in BXD recombinant inbred mice	J Pharmacol Exp Ther	286(1)	263-271	Jul	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9655868&dopt=Abstract	9655868		01				Male	3-58	seizure severity:0= no response; 4 or 5= sever tonic or clonic convulsions; 6 or 7= sever or tonic convulsions after mouse released 	42.65	1.85	77.11	3.44	58	2.64	83.25	3.94	72.21	7.25	33.65	3.99	54.75	5.60	74.69	3.84	65.24	4.50	48.41	3.04	66.86	4.23	49.03	3.63	29.78	11.77	36.19	5.78	30.38	4.05	7.19	1.70			56.1	2.44	58.57	4.73	78.33	0.63	68.42	6.98	59.71	9.10	58.86	4.31	46.93	4.65	14.77	2.84	70.25	4.78	5.5	1.75	57.88	4.60																							6/19/2003	MK Sullivan		ETHIC(VAP)	AREA25	AREA25      ETMEAN	EtOH	1.5 mg/ml blood	RI-106	JCC	p. 267, Fig 7	EQ 2/9/00 and JD 020702	9655868.01
Area under the 25-hr curve for withdrawal following 72 hr exposure to air. Pyrazole injections were given daily to inhibit EtOH metabolism. Handling-induced convulsions (HIC) were scored hourly for 10 hr and again at hrs 24 and 25 [seizure severity]		Male mice from C57BL/6J (B6), DBA/2J (D2) and their 25 recombinant inbred (RI) strains were exposed to ethanol (EtOH) vapor (3.0-9.0 mg EtOH/liter of air) for 72 hr. Mice were selected such that each strain averaged 1.34 to 1.59 mg of EtOH/ml of blood on withdrawal. Control groups and EtOH-exposed groups were tested hourly for handling-induced convulsions (HIC) for 10 hr and at hr 24 and 25. Strain withdrawal severity was indexed as the area under the 25-hr HIC curve for the EtOH group minus that strain's equivalent value for the control group. Genome-wide quantitative trait locus (QTL) analyses correlating strain means with allelic status at > 1500 markers identified 10 chromosomal regions at P < .01. These provisionally identified QTLs were on chromosomes 1 (2 QTLs), 3, 9 (2 QTLs), 10, 12, 13, 15 and 18. Multiple regression analysis using the four most influential QTLs revealed that these loci controlled 86% of the genetic variance. A QTL mapped to distal chromosome 1 (P < .001) is in the same region as one previously definitively mapped for acute alcohol withdrawal, as well as one mapped for acute pentobarbital withdrawal. Several of the QTLs map near potential candidate genes. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Crabbe JC 	Provisional mapping of quantitative trait loci for chronic ethanol withdrawal severity in BXD recombinant inbred mice	J Pharmacol Exp Ther	286(1)	263-271	Jul	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9655868&dopt=Abstract	9655868		02				Male	3-24	seizure severity:0= no response; 4 or 5= sever tonic or clonic convulsions; 6 or 7= sever or tonic convulsions after mouse released 	9.9	1.90	15.54	3.69	29.19	4.24	7.72	2.84	39	4.73	1.71	0.92	38.58	5.23	24	3.99	6.06	3.78	24.33	5.93	35.38	6.68	4.28	1.55	2.21	1.40	2.67	0.71	3.5	1.94	0	0			10.85	3.74	13.57	5.42	4.83	0.64	3.19	1.71	0.67	0	8.31	2.10	5.33	1.71	0.08	0	31.22	3.99	0.22	0	0.29	0																							6/19/2003	MK Sullivan		PYRHIC68.1(VAP)	PYRAREA25	PYRAREA25  SALMEAN	Air/Pyrazole		RI-106	JCC	p. 267, Fig 7	EQ 2/9/00 and JD 020702	9655868.02
EtOH withdrawal severity corrected for differences in HIC (handling-induced convulsions) response to pyrazole. Difference between strain mean values for AREA25 and PYRAREA25 [seizure severity]		Male mice from C57BL/6J (B6), DBA/2J (D2) and their 25 recombinant inbred (RI) strains were exposed to ethanol (EtOH) vapor (3.0-9.0 mg EtOH/liter of air) for 72 hr. Mice were selected such that each strain averaged 1.34 to 1.59 mg of EtOH/ml of blood on withdrawal. Control groups and EtOH-exposed groups were tested hourly for handling-induced convulsions (HIC) for 10 hr and at hr 24 and 25. Strain withdrawal severity was indexed as the area under the 25-hr HIC curve for the EtOH group minus that strain's equivalent value for the control group. Genome-wide quantitative trait locus (QTL) analyses correlating strain means with allelic status at > 1500 markers identified 10 chromosomal regions at P < .01. These provisionally identified QTLs were on chromosomes 1 (2 QTLs), 3, 9 (2 QTLs), 10, 12, 13, 15 and 18. Multiple regression analysis using the four most influential QTLs revealed that these loci controlled 86% of the genetic variance. A QTL mapped to distal chromosome 1 (P < .001) is in the same region as one previously definitively mapped for acute alcohol withdrawal, as well as one mapped for acute pentobarbital withdrawal. Several of the QTLs map near potential candidate genes. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Crabbe JC 	Provisional mapping of quantitative trait loci for chronic ethanol withdrawal severity in BXD recombinant inbred mice	J Pharmacol Exp Ther	286(1)	263-271	Jul	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9655868&dopt=Abstract	9655868		03				Male	3-58	seizure severity:0= no response; 4 or 5= sever tonic or clonic convulsions; 6 or 7= sever or tonic convulsions after mouse released 	32.75	1.90	61.57	3.48	29.01	2.46	75.53	3.94	33.21	3.52	31.94	4.05	16.17	5.36	50.69	3.87	59.17	4.57	24.08	3.09	31.48	4.18	44.76	3.54	27.56	11.60	33.52	5.67	26.88	4.00	7.19	1.87			45.25	2.30	45	4.67	73.5	0.79	65.24	7.11	59.05	8.97	50.56	4.30	41.6	4.03	14.69	2.94	39.03	4.64	5.28	1.56	57.58	4.48																							6/19/2003	MK Sullivan		ETHIC(VAPdelta)	DELAREA25	DELAREA25  WDR              DIFFAR	EtOH	1.5 mg/ml blood	RI-106	JCC	p. 267, Fig 8	EQ 2/9/00 and JD 020702	9655868.03
Locomotor activity.  Corn Oil, 30 minute test.		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		02	7 wks	49		Male			46.7		46.2		57.3		33.2		27		52.5		36.1				30.9		39.3		31.6		49.1		31.2		31.7		39		44.4				40.8						25.3		40.9		33.3		24.1		55.9		31.3		36.8		41.6																								12/26/2002			OILACT		OILACT	Corn Oil	10ml/kg		FOR	p. 671, Fig 1	MRG with FOR from files and publication 021402	11106859.02
Locomotor activity.  Paraoxon, 30 minute test.		Genetic mechanisms responsible for  organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		01	7 wks	49		Male			29		14.2		26.3		42.6		14.4		39		24.3				14.9		20.4		11.4		33.8		16.7		15.1		31.3		22.7				17.1						9.9		24.7		26.6		12.5		36.6		25		15		12.2																								12/26/2002			PARAOX		PARAOX	Paraoxon	0.25mg/kg		FOR	p. 671, Fig 1	MRG with FOR from files and publication 021402	11106859.01
54 degree C hot plate latencies baseline (before 3 min forced swim in 15 degree C water) MF [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	01	8-12 wks	56	96	MF	9-26	seconds	19.1	1.2	24.3	1.6	22.6	 0.9	19.4	1.6	18.3	1.7	19.8	1.8	28.6	2.1	19.8	2.1	18.1	1.7	24.5	1.7	23.9	2.3	24.6	2.2	18.3	1.6	15.1	1.5	25.9	1.7	16.1	1.5			20.9	1.5	24.6	3.2	15.9	2.1			24.2	2.0	20.4	1.8	18.3	1.3	17.9	1.3	18.9	1.1	13	1.1	13.6	1.2																							7/3/2003	MK Sullivan											9315917.01
54 degree C hot plate latencies baseline (before 3 min forced swim in 15 degree C water), Female [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	02	8-12 wks	56	96	Female	3-10	seconds	20.5	1.4	22.2	2.4	21.4	0.6	20	2.4	17.1	2.3	19.9	2.9	27.3	2.8	16.3	2.2	14.9	1.7	26	2.8	21.3	2.2	18.7	1.2	16.5	2.7	15.9	0.6	23.6	2.7	15.2	2.3			20.7	2.7	17.3	5.5	13.5	2.1			19.5	2.1	21.3	1.9	17.4	1.7	16.9	1.9	18	1.6	12.6	1.3	12.4	1.3																							7/3/2003	MK Sullivan											9315917.02
54 degree C hot plate latencies baseline (before 3 min forced swim in 15 degree C water), Male [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	03	8-12 wks	56	96	Male	4-18	seconds	17.5	1.9	26.1	2.0	23.7	1.7	18.9	2.1	19.8	2.5	19.7	2.2	30.5	3.2	26.6	1.9	22.1	2.6	23	2.1	26.6	4.0	29.7	2.8	20.3	1.6	14.1	3.2	27.4	2.1	17	1.9			21	1.4	28.2	3.2	18.2	3.5			27.9	2.8	19.5	3.3	19.2	1.9	18.8	1.8	19.9	1.6	13.3	1.7	14.7	2.0																							7/3/2003	MK Sullivan											9315917.03
54 degree C hot plate latencies Post-Swim MF [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	04	8-12 wks	56	96	MF	9-26	seconds	46.5	4.3	42.5	3.9	58.2	1.2	32.5	3.8	48.2	4..8	50.6	3.0	52.1	3.5	55.5	3.1	52.5	3.6	55.1	2.1	60	0	35.8	4.6	43.9	3.6	49.6	3.6	51.5	3.0	33.1	3.1			56.4	3.2	44.2	6.5	37	4.0			54.9	2.6	54.5	2.3	50.7	3.3	33.4	4.0	34.2	5.0	24.6	4.2	41.4	3.3																							7/3/2003	MK Sullivan											9315917.04
54 degree C hot plate latencies Post-Swim Female [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	05	8-12 wks	56	96	Female	3-10	seconds	46.7	5.0	39.1	4.5	58.1	1.9	29.6	3.2	51.6	5.9	51.3	4.4	54.2	3.3	53.2	4.4	54.5	3.8	55.4	3.3	60	0	30	7.5	39.4	5.7	50.2	5.1	47.7	6.2	34.0	4.4			60	0	31.7	14.2	31.5	5.5			57.1	2.9	60	0	47.1	4.4	33.4	5.2	28	6.1	14.7	2.4	44.4	4.6																							7/3/2003	MK Sullivan											9315917.05
54 degree C hot plate latencies Post-Swim Male [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	06	8-12 wks	56	84	Male	4-18	seconds	46.2	7.7	45.6	6.3	58.3	1.7	35.1	6.6	44.2	8.0	49.9	4.4	49.1	7.2	60.0	0.0	49.8	7.0	54.7	2.7	60.0	0.0	40.9	5.5	48.8	3.8	48.8	5.5	53.9	3.1	32.1	4.5			52.7	6.3	50.5	6.0	42.6	5.5			53.2	4.1	48.9	3.8	54.3	4.8	33.5	6.2	40.1	7.7	32.3	6.2	38.6	4.8																							7/3/2003	MK Sullivan											9315917.06
Acoustic startle response to a 110 dB SPL, 10 kHz tone without prepulse stimulus[g]		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R 	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	06	100 days	100		MF	9-15	g	23.6		14.1		23.5				10.7		30.7		10.3		5.6		17.2		14.2		16.3		18.3		14.4		26.2		6.7		18.9				7.9		7.9		2.1		26.4		14.2		57.3		10.6		24.7		15.1		20.7		18.1																								6/6/2002	Ryan McNeive	Ryan McNeive										10371755.06
High frequency hearing loss and cochlear pathology; Acoustic startle response to 10 kHz white-noise bursts at 100 dB [g]		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	02	100 days	100		MF	9-15	g	14.7		10.2		6.7				5.2		19.4		6.2		2.1		6		11.5		6.4		4.9		11		13.9		2.5		9.4				1.8		3.4		1.3		10.8		3.8		42.2		10		4		11.7		7.6		4.7																								12/26/2002	Ryan McNeive	Ryan McNeive										10371755.02
High frequency hearing loss and cochlear pathology; Acoustic startle response to 20 kHz white-noise bursts at 100 dB [g] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	04	100 days	100		MF	9-15	g	9.1		6.3		6.4				3.4		13		2.1		2.2		6.4		10.6		5.2		8.5		8.6		14.7		2		4.7				5.5		4.1		1.2		11		3.6		31.6		7.4		3.6		17.4		7.8		2.1																								12/26/2002	Ryan McNeive	Ryan McNeive										10371755.04
High frequency hearing loss and cochlear pathology; Acoustic startle response to  5 kHz white-noise bursts at 100 dB SPL [g] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	01	100 days	100		MF	9-15	g	0.3		1.1		0.4				0.4		5.3		2.8		0.1		1.5		2.7		0.8		-0.1		1.8		4.9		0.1		6.4				-0.5		0.8		0.8		1.7		-0.4		8.8		-1		0.6		0.1		0.5		1.7																								12/26/2002	Ryan McNeive	Ryan McNeive										10371755.01
High frequency hearing loss and cochlear pathology; Acoustic startle response to 15 kHz white-noise bursts at 100 dB SPL [g] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	03	100 days	100		MF	9-15	g	21.4		7.3		9.9				5.1		14.8		2		2.4		8.8		10		5.2		10.4		7.6		18.1		4.6		7.8				3.6		5		1		15.4		5.2		39.5		7.4		3.4		24.9		9.9		3.6																								12/26/2002	Ryan McNeive	Ryan McNeive										10371755.03
High frequency hearing loss and cochlear pathology; Acoustic startle response to 25 kHz white-noise bursts at 100 dB SPL [g] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	05	100 days	100		MF	9-15	g	2.9		1.8		2.4				2		3.4		-0.4		1.4		2.1		4.1		2.2		1		4.6		10.4		0.9		1.4				-0.2		0.6		-0.5		-0.2		1.2		16		0.2		1.4		4.4		2.5		-0.8																								12/26/2002	Ryan McNeive	Ryan McNeive										10371755.05
High frequency hearing loss and cochlear pathology; Acoustic startle response to white-noise bursts at 110 dB SPL [g] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	07	100 days	100		MF	9-15	g	24.3		7.4		14.5				11.7		23.5		12.1		7.5		15.9				10.9		12.4		13.2		21.1		2.6		17.1				2.1		5.5		3.6		20.2		11.3		47.1		12.1		10.1		21.3		16.4		20.9																								6/6/2002	Ryan McNeive	Ryan McNeive										10371755.07
Alcohol acceptance total consumption over 24 hr female [g/kg]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains.	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	01	71-91 days	71	91	Female	8-20	g/kg	20.21		9.18		15.99		15.76		19.37		17.07		12.32		11.03		18.78		116.25		14.88		18.6				21.47		13.51						21.97		15.52				10.85		12.45		10.88		9.63		15.71				18.19		10.39																								7/11/2003	MK Sullivan		ACCB alcohol acceptance									7695038.01
Alcohol acceptance total consumption over 24 hr male [g/kg]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains.	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	02	71-91 days	71	91	Male	7-21	g/kg	16.84		10.22		16.1		14.96		15.26		13.48		11.46		7.73		16.78		14.43		10.03		10.35				14.77		7.08						16.47		14.66				5.12		11.71		12.06		11.73		15.57				15.58		12																								7/11/2003	MK Sullivan		ACCB alcohol acceptance									7695038.02
Alcohol acceptance - consumption of 10% ethanol in 24 hours after 24 hours of water deprivation [g/kg]		Quantitative trait loci (QTL) mapping of complex phenotypes has emerged as an important feature of the recombinant inbred (RI) strain methodology. In this second study of our series on alcohol-related behaviors in mice, we examine alcohol acceptance, preference, and hypnotic dose sensitivity (HDS) to a standard dose of alcohol measured in BXD RI strains to identify candidate QTL regions responsible for their heritability. We detected highly significant marker associations for acceptance on chromosome 12 (Eif4e), for preference on chromosome 1 (D1Rti2) and chromosome 7 (D7Mit7), and for HDS on chromosome 7 (Mpmv1). These are the strongest QTL associations that we detected, but several other candidate QTL regions are reported. Given the limited number of BXD RI strains available, the large number of markers used herein, and the consequent chance of identifying false marker associations, these RI QTL mapping results must be seen as tentative, but an important first step toward identifying QTL for alcohol-related behaviors.	Rodriguez LA,Ê Plomin R,ÊBlizard DA,ÊJones BC,Ê McClearn GE.	Alcohol acceptance, preference, and sensitivity in mice. II. Quantitative trait loci mapping analysis using BXD recombinant inbred strains.	Alcohol Clin Exp Res	19(2)	367-373	Apr	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625571&dopt=Abstract	7625571	95351511	01	71-91 days	71	91	MF	17-41	g/kg	18.48		9.71		16.05		15.41		17.43		15.37		11.86		9.38		17.67		15.34		12.45		14.48				18.12		10.3						19.08		15.11				7.98		12.1		11.47		10.68		15.64				16.88		11.24																								7/11/2003	MK Sullivan		ETLORR4.1(PSU)	Acceptance	ACCEPT	EtOH	0.1		Rodriguez	p. 369, Table 1	MRG 120601 from publication	7625571.01
Alcohol acceptance - male raw mean consumption [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		02	74-91 days	74	91	Male	~50	g/kg body weight     					16.10		14.96		15.26		13.48		11.28		9.47		16.78		14.75		10.03		10.40				14.77		7.08		10.92				16.47		14.66				4.85		13.25		12.06		11.73		15.57		9.38		15.58		11.02																								6/5/2003	MK Sullivan	Nathan Copeland	ACCB alcohol acceptance									10581484.02
Alcohol acceptance - female raw mean consumption [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		03	74-91 days	74	91	Female	~50	g/kg body weight     					15.99		15.76		18.53		17.07		12.59		12.75		18.78		16.25		14.75		18.84				21.47		1351		15.41				18.35		15.70				10.10		13.48		10.88		9.63		17.43		12.82		18.18		11.05																								6/5/2003	MK Sullivan	Nathan Copeland	ACCB alcohol acceptance									10581484.03
Alcohol acceptance - male residual [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		01	74-91 days	74	91	Male	~50	g/kg body weight     					2.97		1.98		0.46		-0.36		0.39		-1.53		1.82		1.44		-2.28		-4.46				-1.97		-4.42		-1.83				1.78		1.72				-4.40		1.77		2.29		2.79		1.49		-1.67		1.00		1.15																								6/5/2003	MK Sullivan	Nathan Copeland	ACCB alcohol acceptance									10581484.01
Alcohol acceptance - female residual [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		04	74-91 days	74	91	Female	~50	g/kg body weight     					-1.54		-1.00		1.56		1.29		-1.72		-0.34		0.79		-0.37		1.28		5.12				4.83		2.02		1.35				0.58		-0.87				0.09		-2.14		-3.95		-4.98		0.26		-0.21		1.00		-3.08																								6/5/2003	MK Sullivan	Nathan Copeland	ACCB alcohol acceptance									10581484.04
Alcohol preference - female [g/kg]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	03	50-70 days	50	70	Female	8-20	avg g/kg	16.92		2.64		5.56		6.51		4.59		8.03		4.28		3.33		4.98		4.81		2.4		3.2				9.61		4.06						4.7		4.29				3.15		7.95		8.39		6.63		3.91				10.49		2.19																								7/11/2003	MK Sullivan											7695038.03
Alcohol preference - male [g/kg]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	04	50-70 days	50	70	Male	9-21	avg g/kg	12.84		2.07		3.32		3.65		3.68		4.69		4.98		2.64		5.05		5.2		2.03		2.15				4.08		2.18						4.57		3.73				2.34		7.25		6.37		6.84		5.06				8.04		2.32																								7/11/2003	MK Sullivan											7695038.04
alcohol preference - consumption of 10% ethanol vs. water over 15 days [g/kg]		Quantitative trait loci (QTL) mapping of complex phenotypes has emerged as an important feature of the recombinant inbred (RI) strain methodology. In this second study of our series on alcohol-related behaviors in mice, we examine alcohol acceptance, preference, and hypnotic dose sensitivity (HDS) to a standard dose of alcohol measured in BXD RI strains to identify candidate QTL regions responsible for their heritability. We detected highly significant marker associations for acceptance on chromosome 12 (Eif4e), for preference on chromosome 1 (D1Rti2) and chromosome 7 (D7Mit7), and for HDS on chromosome 7 (Mpmv1). These are the strongest QTL associations that we detected, but several other candidate QTL regions are reported. Given the limited number of BXD RI strains available, the large number of markers used herein, and the consequent chance of identifying false marker associations, these RI QTL mapping results must be seen as tentative, but an important first step toward identifying QTL for alcohol-related behaviors.	Rodriguez LA,Ê Plomin R,ÊBlizard DA,ÊJones BC,Ê McClearn GE.	Alcohol acceptance, preference, and sensitivity in mice. II. Quantitative trait loci mapping analysis using BXD recombinant inbred strains.	Alcohol Clin Exp Res	19(2)	367-373	Apr	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625571&dopt=Abstract	7625571	95351511	02	50-70 days	50	70	MF	18-41	g/kg	14.83		2.35		4.44		5.08		4.13		6.36		4.67		2.98		5.02		5		2.22		2.7				6.54		3.07						4.64		4.01				2.72		7.6		7.83		6.73		4.49				9.27		2.25																								7/11/2003	MK Sullivan		ACCB alcohol acceptance	Preference	PREFER	EtOH	0.1		Rodriguez	p. 369, Table 1	MRG 120601 from publication	7625571.02
Alcohol preference - male raw mean consumption [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		05	53-67 days	53	67	Male	~50	g/kg body weight     					3.31		3.60		3.68		4.66		3.82		2.68		5.75		4.82		1.97		2.27				4.09		2.22		4.43				4.46		3.68				2.22		6.54		5.64		5.53		5.04		3.01		8.01		2.37																								6/5/2003	MK Sullivan	Nathan Copeland										10581484.05
Alcohol preference - female raw mean consumption [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		06	53-67 days	53	67	Female	~50	g/kg body weight     					5.36		6.48		4.09		6.73		4.91		2.96		5.02		4.82		2.25		3.49				11.03		4.05		4.98				4.62		4.19				3.18		6.90		8.38		6.59		3.84		4.78		10.44		2.22																								6/5/2003	MK Sullivan	Nathan Copeland										10581484.06
Alcohol preference - male residual mean [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		07	53-67 days	53	67	Male	~50	g/kg body weight     					-0.81		-1.05		0.16		-0.10		-0.09		-0.31		1.79		0.96		-0.68		-0.97				-1.18		0.49		0.69				0.69		0.11				-0.88		1.70		0.10		0.83		1.64		-0.83		1.50		-0.27																								6/5/2003	MK Sullivan	Nathan Copeland										10581484.07
Alcohol preference - female residual mean [g/kg body weight]		During the past half century, researchers have identified and examined sex differences in alcohol-related phenotypes, focusing more recently on understanding of the mechanisms underlying these differences. In general, the genetic contributions influencing these differences are not consistent with an interpretation of sex linkage and must, therefore, reflect some form of sex limitation in which allelic differences at particular autosomal loci have different consequences in males and females. Significant sex differences in measures of alcohol consumption in mice have been demonstrated in previous work in our laboratory. To investigate these differences further, we explore the limiting case of sex-exclusive effects using data from (BXD) recombinant inbred (RI) strains of mice and from an intercross derived from the same progenitors, C57BL/6J (B) and DBA/2J (D). By the use of two statistical approaches (examination of residual scores as a sex-exclusive phenotypic value for the RI strains and multivariate regression on sex and genotype in the F(2)) we have identified and confirmed female-exclusive markers for alcohol acceptance on chromosomes 9 and 12 and one marker for alcohol preference on chromosome 2. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:647-652, 1999. Copyright 1999 Wiley-Liss, Inc.	Fernandez JR, Vogler GP, Tarantino LM, Vignetti S, Plomin R, McClearn GE	Sex-exclusive quantitative trait loci influences in alcohol-related phenotypes	Am J Med Genet 	88(6)	647-652	Dec	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10581484&dopt=Abstract	10581484		08	53-67 days	53	67	Female	~50	g/kg body weight     					0.88		1.70		-0.77		0.85		-0.10		-0.87		-1.98		-1.22		-0.85		0.09				5.75		0.70		-0.66				-1.05		-0.67				-0.17		-0.92		1.49		-0.18		-2.43		0.61		1.09		-1.29																								6/5/2003	MK Sullivan	Nathan Copeland										10581484.08
Antinociceptive responsiveness [%] 		Among inbred mouse strains, DBA/2 mice are unique because of their poor responsiveness to nitrous oxide (N2O) antinociception. As a first step towards identifying candidate genes involved in determining antinociceptive responsiveness to N2O, male mice from the DBA/2 strain, the more responsive C57BL/6 strain, their B6D2F1 offspring, and 22 BXD recombinant inbred (RI) strains derived from DBA/2 and C57BL/6 mice were exposed to N2O and evaluated using the acetic acid abdominal constriction test. When exposed to 70% N2O, C57BL/6, DBA/2 and B6D2F1 mice exhibited antinociceptive responses of 78, 22 and 55%, respectively. The BXD RI strains demonstrated varying degrees of responsiveness to N2O. Cluster analysis revealed one cluster of 16 strains approximating the C57BL/6 progenitor (61.9-100% antinociceptive response to 70% N2O) and another of six strains around the DBA/2 progenitor (9.1-40% antinociceptive response to 70% N2O). The robust strain differences permitted screening the strain means with 1492 marker loci previously mapped in BXD RI strains. Using a QTL analysis specifically tailored to existing mouse RI strains, we found associations at the 0.01 level on seven chromosomes with the most promising marker loci being Il2ra, Hbb, Hmg1rs7 and Gsl5 on chromosomes 2, 7, 16 and 19, respectively (P < 0.002).	Quock RM, Mueller JL, Vaughn LK, Belknap JK	Nitrous oxide antinociception in BXD recombinant inbred mouse strains and identification of quantitative trait loci.	Brain Research	725(1)	23-29	June	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8828582&dopt=Abstract	8828582	96426288	01	6-7wks	42	49	Male	5	%	77		27		87		70		94				37		80		40		85		60		100		80		74				30				31		96				89		100		10		90		70		24		90		70																								6/10/2003	MK Sullivan											8828582.01
Audiogenic seizure susceptibility at 21 days [severity of seizure] 		Recombinant inbred (RI) strains are valuable not only for detecting major gene segregation and linkage but also for identifying associations between behavior and quantitative trait loci (QTL) that account for relatively small amounts of variation in behaviors for which strain distribution patterns are not bimodal. When applied to published data on genetic markers and on behavior for BXD RI strains, the RI QTL association approach suggests the presence of QTLs on chromosomes 6 and 12 for open-field activity and on chromosomes 1, 2, and 17 for high-pressure seizure susceptibility. Because the RI QTL approach does not require that the progenitor inbred strains of a particular RI series differ, researchers could focus on the BXD RI series, for which the greatest number of genetic markers are available. Focusing on BXD would capitalize on the cumulative nature of RI research which permits analyses of QTL sources of genetic correlations across studies.	Plomin R, McClearn GE, Gora-Maslak G,Ê Neiderhiser JM.	Use of recombinant inbred strains to detect quantitative trait loci associated with behavior.	Behav Genet	277(2)	99-116	Mar	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2049054&dopt=Abstract	2049054	91264768	01	21 days	21				Severity of seizure; 0=no response, 1=wild running, 2=clonic seizure, 3=tonic seizure	.25		2.75		.25		2.25		2.25		.25		1.75		2.75		1.25		.25		.25		.25		2.75		.25				1.25				2.75				1.25		1.25		.25		1.75		1.25		.25		.25																												7/14/2003	MK Sullivan											2049054.01
Response to auditory stimulus US in contextualized fear conditioning paradigm [% freezing]		Fear conditioning shows associations formed between contextual or auditory stimuli with an unconditioned stimulus. Inbred mouse strains differ in their ability to demonstrate fear conditioning, suggesting at least a partial genetic influence. The present study identified the possible chromosomal loci regulating fear conditioning in BXD recombinant inbred strains using quantitative trait loci (QTL) analysis. Estimates of heritability for all 3 measures of conditioning were about .28. Correlational analyses between genetic markers and strain means identified multiple putative QTLs. The strongest associations were on Chromosomes 1 and 17 for freezing to the context, Chromosome 12 for freezing to an altered context, and Chromosome 1 for freezing to the auditory stimulus. Overlapping QTLs may indicate some common genes that underlie aspects of this learning task.	Owen EH, Christensen SC, Paylor R, Wehner JM	Identification of quantitative trait loci involved in contextual and auditory-cued fear conditioning in BXD recombinant inbred strains.	Behav Neurosci 	111(2)	292-300	Apr	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9106670&dopt=Abstract	9106670	97260550	01	60-134 days 	60	134	MF	9-20	% freezing	70	5.62	60	5.46	62	5.38	45	7.15			20	4.38	51	7.62	60	5.23	100	1.23	40	6.62	64	6.38	32	5.00			18	4.54			20	5.23			67	8.62	61	3.90	64	3.77	41	9.15	50	5.92	53	5.77	61	5.31	64	6.54	62	5.38			65	4.62																							6/12/2003	MK Sullivan											9106670.01
Body weight [g]		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	01	106 days	106		MF	8-35	g	21.2		20.3		21.1		22.9		19.9		19.3		19.3		23.4		21		18.8		21.8		22.8		23.6		22		21		18.7		17.9		22.2		21.7		18.5		21.8		17.5		19.6		21.8		19		17.3		22.1		22																								6/12/2003	MK Sullivan											10102277.01
Brain methamphetamine levels after 8 mg/kg methamphetamine [micrograms/gm] 		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains.	J Neurosci	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	09	10-14 wks	70	98	MF	8	micrograms/gm	2	0.39	2.5	0.64	3.8	0.96	1.5	0.31	2.1	0.23	1.9	0.32	2.9	0.60	2.5	0.46	2.7	0.74	2.7	0.43	2.7	0.47	3.8	0.62	2.8	0.71	1.8	0.39	2.1	0.51	2.9	0.88			2.1	0.63	1.8	0.26	2.3	0.40	1.9	0.41	0.8	0.19	2	0.60	2.7	0.79	2	0.80	2.5	0.55	2.8	0.59	2.1	0.71																							6/4/2003	MK Sullivan											8987796.09
Brain weight [mg]		Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells.	Williams RW, Strom RC., Goldowitz D 	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	J Neurosci	18(1)	138-46	Jan	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9412494&dopt=Abstract	9412494	98075112	01	100 days	100		MF	5-11	mg	475		412		465		432		526		388		412		422		437		434		427		442		443		469		427		431		398		443		457		434		391		431		393		407		413		399		426		434																								6/18/2003	MK Sullivan											9412494.01
Brain weight [mg] [strains 33 to 42 calculated 6/28/00]		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	02	106 days	106		MF	8-35	mg	475		412		465		432		526		388		412		422		437		434		427		442		443		469		427		431		398		443		457		434		391		431		393		407		413		399		426		434		427.3		417.3		415.4		406.6		410.6		418.1		401.8		431.7				448.6				6/12/2003	MK Sullivan											10102277.02
Bronchial constrictor response- after exposure to atracurium [APTI (airway pressure time index)] [cmH2O.s]		Asthma is a complex heritable inflammatory disorder of the airways associated with clinical signs of atopy and bronchial hyperresponsiveness. Recent studies localized a major gene for asthma to chromosome 5q31-q33 in humans. Thus, this segment of the genome represents a candidate region for genes that determine susceptibility to bronchial hyperresponsiveness and atopy in animal models. Homologs of candidate genes on human chromosome 5q31-q33 are found in four regions in the mouse genome, two on chromosome 18,Êand one each on chromosomes 11Êand 13.ÊWe assessed bronchial responsiveness as a quantitative trait in mice and found it linked to chromosome 13.ÊInterleukin 9Ê(IL-9) is located in the linked region and was analyzed as a gene candidate. The expression of IL-9 was markedly reduced in bronchial hyporesponsive mice, and the level of expression was determined by sequences within the qualitative trait locus (QTL). These data suggest a role for IL-9 in the complex pathogenesis of bronchial hyperresponsiveness as a risk factor for asthma. 	Nicolaides NC, Holroyd KJ, Ewart SL, Eleff SM, Kiser MB, Dragwa CR, Sullivan CD, Grasso L, Zhang LY, Messler CJ, Zhou T, Kleeberger SR, Buetow KH, Levitt RC.	Interleukin 9: a candidate gene for asthma.	Proc Natl Acad Sci USA 	94(24)	13175-13180	Nov	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9371819&dopt=Abstract	9371819		01	5-6 wks	35	42	MF	2-13	cmH20.s	86	18	404	40	109	15	142	15	65	11	169	8	247	26	273	22	107	10	408	33	281	40	53	13	462	203	521	115	164	13	84	21			317	47	54	24			83	13	984	125	570	120	291	14	102	23	346	48	304	21	142	15																							6/11/2003	MK Sullivan	Nathan Copeland										9371819.01
Quiescent stem cells in old mice-cobblestone area forming cells (CAFC) day 35 frequency in bone marrow [105 BM cells]		To address the fundamental question of whether or not stem cell populations age, we performed quantitative measurements of the cycling status and frequency of hematopoietic stem cells in long-lived C57BL/6 (B6) and short-lived DBA/2 (DBA) mice at different developmental and aging stages. The frequency of cobblestone area-forming cells (CAFC) day-35 in DBA fetal liver was twofold to threefold higher than in B6 mice, and by late gestation, the total stem cell number was nearly as large as that of young DBA adults. Following a further approximately 50% increase in stem cells between 6 weeks and 1 year of age, numbers in old DBA mice dropped precipitously between 12 and 20 months of age. In marked contrast, this stem cell population in B6 mice increased at a constant rate from late gestation to 20 months of age with no signs of abatement. Throughout development an inverse correlation was observed between stem cell numbers and the percentage of cells in S-phase. Because a strong genetic component contributed to the changes in stem cell numbers during aging, we quantified stem cells of 20-month old BXD recombinant inbred (RI) mice, derived from B6 and DBA progenitor strains, thus permitting detailed interstrain genetic analysis. For each BXD strain we calculated the stem cell increase or decrease as mice aged from 2 to 20 months. Net changes in CAFC-day 35 numbers among BXD strains ranged from an approximately 10-fold decrease to an approximately 10-fold increase. A genome-wide search for loci associated with this quantitative trait was performed. Several loci contribute to the trait-putative loci map to chromosomes X, 2, and 14. We conclude that stem cell numbers fluctuate widely during aging and that this has a strong genetic basis.	de Haan G, Van Zant G	Dynamic changes in mouse hematopoietic stem cell numbers during aging.	Blood	93(10)	3294-3301	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233881&dopt=Abstract	10233881	99252083	01	2 months	60	62	Female		105 BM cells	1.5		3		1.5						2				3.5		8		2				3		2		2.5		2.5		2		2						2		2		1		2		3		0.5		3		3.3		3.5																								6/9/2003	MK Sullivan											10233881.01
Quiescent stem cells in aged mice-cobblestone area forming cells (CAFC) day 35 frequency in bone marrow [105 BM cells]		To address the fundamental question of whether or not stem cell populations age, we performed quantitative measurements of the cycling status and frequency of hematopoietic stem cells in long-lived C57BL/6 (B6) and short-lived DBA/2 (DBA) mice at different developmental and aging stages. The frequency of cobblestone area-forming cells (CAFC) day-35 in DBA fetal liver was twofold to threefold higher than in B6 mice, and by late gestation, the total stem cell number was nearly as large as that of young DBA adults. Following a further approximately 50% increase in stem cells between 6 weeks and 1 year of age, numbers in old DBA mice dropped precipitously between 12 and 20 months of age. In marked contrast, this stem cell population in B6 mice increased at a constant rate from late gestation to 20 months of age with no signs of abatement. Throughout development an inverse correlation was observed between stem cell numbers and the percentage of cells in S-phase. Because a strong genetic component contributed to the changes in stem cell numbers during aging, we quantified stem cells of 20-month old BXD recombinant inbred (RI) mice, derived from B6 and DBA progenitor strains, thus permitting detailed interstrain genetic analysis. For each BXD strain we calculated the stem cell increase or decrease as mice aged from 2 to 20 months. Net changes in CAFC-day 35 numbers among BXD strains ranged from an approximately 10-fold decrease to an approximately 10-fold increase. A genome-wide search for loci associated with this quantitative trait was performed. Several loci contribute to the trait-putative loci map to chromosomes X, 2, and 14. We conclude that stem cell numbers fluctuate widely during aging and that this has a strong genetic basis.	de Haan G, Van Zant G	Dynamic changes in mouse hematopoietic stem cell numbers during aging.	Blood	93(10)	3294-3301	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233881&dopt=Abstract	10233881	99252083	02	20 months	600	620	Female		105 BM cells	4		1		1						12				11.5		2		4.5				7		21		3.3		6		3.3		4						2.5		2.5		6		4		4		0.1		6.5		2		3.5																								6/9/2003	MK Sullivan											10233881.02
Chlordiazepoxide 10 mg/kg induced locomotor response distance traveled, 0-5 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	01	8-12 wks	56	84	Male	3-15	cm	-696	292	-81	123	-716	282			-40	182	-9	448	-284	391	197	163	919	668	112	156	-509	310	-594	250	216	233	7	239	668	276	335	299	744	295	76	115	787	282	-113	208	739	317	-39	304	-413	337	387	280	742	291	204	328	328	268	299	200																							6/6/2003	MK Sullivan											9880575.01
Chlordiazepoxide 10 mg/kg induced locomotor response distance traveled, 5-10 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	02	8-12wks	56	84	Male	3-15	cm	-459	253	863	307	-248	283			-487	209	-36	410	-18	446	-1623	286	1166	246	1306	119	-451	365	132	370	-1104	304	1377	407	10	431	-39	228	510	505	-246	299	-448	295	256	545	174	393	-86	294	-497	574	409	278	1909	316	-590	283	527	331	500	370																							6/6/2003	MK Sullivan											9880575.02
Chlordiazepoxide 10 mg/kg induced locomotor response distance traveled, 10-15 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	03	8-12wks	56	84	Male	3-15	cm	-69	352	875	219	-462	245			-846	231	-137	413	-285	269	-2600	262	518	381	477	773	-642	239	443	414	-1036	171	1013	337	266	372	-403	306	453	487	-520	255	-743	297	104	378	-390	370	-110	345	-555	658	9	170	903	362	-28	281	774	305	419	345																							6/6/2003	MK Sullivan											9880575.03
Chlordiazepoxide 10 mg/kg induced locomotor response distance traveled, 15-20 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	04	8-12wks	56	84	Male	3-15	cm	297	156	857	293	-817	248			-705	170	-358	318	-425	269	-2564	356	319	284	-383	707	-888	242	268	390	-835	359	814	387	367	347	-828	309	-40	420	-354	319	-622	335	825	552	-351	206	-132	365	-1058	181	-340	206	1059	399	-312	160	233	371	504	314																							6/6/2003	MK Sullivan											9880575.04
Chlordiazepoxide 10 mg/kg induced locomotor response distance traveled, 5-20 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	05	8-12wks	56	84	Male	3-15	cm	-231	761	2595	819	-1526	776			-2039	610	-531	1141	-727	985	-6786	903	2002	911	1401	1600	-1981	846	843	1174	-2974	833	3204	1131	643	1149	-1270	843	923	1412	-1119	873	-1812	926	1185	1475	-567	969	-327	1005	-2110	1413	78	653	3870	1077	-930	724	1534	1007	1423	1030																							6/6/2003	MK Sullivan											9880575.05
Cerebellum weight [mg] 		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		01	30-300 days	30	300	MF	4-7	mg					61.4	2.38	49.0	1.25	62.5	2.32	53.1	1.22	59.1	2.07	53.9	1.05	53.1	1.10	45.9	1.09	48.4	1.63	49.4	0.44	47.4	1.15	56.3	1.21	53.6	1.44	50.1	1.42	48.2	1.67	50.6	1.31	53.8	1.51	48.6	1.03	54.9	1.92	49.6	0.81	47.4	2.25	51.5	0.87	50.2	0.56	53.6	1.14	49.7	0.91	56.0	1.19	52.1	0.66	53.7	1.22	49.7	2.03	44.5	0.73			51.1	1.79	54.9	0.87	49.9	1.13			59.4	0.95			12/20/2002												11438585.01
Stem cell cycling - change in day 7 cobblestone area forming cell (CAFC) frequency during aging [%CAFC]		To address the fundamental question of whether or not stem cell populations age, we performed quantitative measurements of the cycling status and frequency of hematopoietic stem cells in long-lived C57BL/6 (B6) and short-lived DBA/2 (DBA) mice at different developmental and aging stages. The frequency of cobblestone area-forming cells (CAFC) day-35 in DBA fetal liver was twofold to threefold higher than in B6 mice, and by late gestation, the total stem cell number was nearly as large as that of young DBA adults. Following a further approximately 50% increase in stem cells between 6 weeks and 1 year of age, numbers in old DBA mice dropped precipitously between 12 and 20 months of age. In marked contrast, this stem cell population in B6 mice increased at a constant rate from late gestation to 20 months of age with no signs of abatement. Throughout development an inverse correlation was observed between stem cell numbers and the percentage of cells in S-phase. Because a strong genetic component contributed to the changes in stem cell numbers during aging, we quantified stem cells of 20-month old BXD recombinant inbred (RI) mice, derived from B6 and DBA progenitor strains, thus permitting detailed interstrain genetic analysis. For each BXD strain we calculated the stem cell increase or decrease as mice aged from 2 to 20 months. Net changes in CAFC-day 35 numbers among BXD strains ranged from an approximately 10-fold decrease to an approximately 10-fold increase. A genome-wide search for loci associated with this quantitative trait was performed. Several loci contribute to the trait-putative loci map to chromosomes X, 2, and 14. We conclude that stem cell numbers fluctuate widely during aging and that this has a strong genetic basis.	de Haan G, Van Zant G	Dynamic changes in mouse hematopoietic stem cell numbers during aging.	Blood	93(10)	3294-3301	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233881&dopt=Abstract	10233881	99252083	03	2-20 months	61	610	Female	3-8	%	110		100		125						110				102		98		105				125		75		110		110		102		104						103		120		100		104		105		90		120		85		80																								6/9/2003	MK Sullivan											10233881.03
Change in day 21 cobblestone area forming cell (CAFC) frequency during aging [% CAFC]		To address the fundamental question of whether or not stem cell populations age, we performed quantitative measurements of the cycling status and frequency of hematopoietic stem cells in long-lived C57BL/6 (B6) and short-lived DBA/2 (DBA) mice at different developmental and aging stages. The frequency of cobblestone area-forming cells (CAFC) day-35 in DBA fetal liver was twofold to threefold higher than in B6 mice, and by late gestation, the total stem cell number was nearly as large as that of young DBA adults. Following a further approximately 50% increase in stem cells between 6 weeks and 1 year of age, numbers in old DBA mice dropped precipitously between 12 and 20 months of age. In marked contrast, this stem cell population in B6 mice increased at a constant rate from late gestation to 20 months of age with no signs of abatement. Throughout development an inverse correlation was observed between stem cell numbers and the percentage of cells in S-phase. Because a strong genetic component contributed to the changes in stem cell numbers during aging, we quantified stem cells of 20-month old BXD recombinant inbred (RI) mice, derived from B6 and DBA progenitor strains, thus permitting detailed interstrain genetic analysis. For each BXD strain we calculated the stem cell increase or decrease as mice aged from 2 to 20 months. Net changes in CAFC-day 35 numbers among BXD strains ranged from an approximately 10-fold decrease to an approximately 10-fold increase. A genome-wide search for loci associated with this quantitative trait was performed. Several loci contribute to the trait-putative loci map to chromosomes X, 2, and 14. We conclude that stem cell numbers fluctuate widely during aging and that this has a strong genetic basis.	de Haan G, Van Zant G	Dynamic changes in mouse hematopoietic stem cell numbers during aging.	Blood	93(10)	3294-3301	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233881&dopt=Abstract	10233881	99252083	04	2-20 months	61	610	Female	3-8	%	180		82		90						200				120		80		125				130		340		108		130		92		130						115		70		110		110		108		60		125		75		108																								6/9/2003	MK Sullivan											10233881.04
Quiescent stem cells - change in day 35 CAFC frequency during aging [% CAFC]		To address the fundamental question of whether or not stem cell populations age, we performed quantitative measurements of the cycling status and frequency of hematopoietic stem cells in long-lived C57BL/6 (B6) and short-lived DBA/2 (DBA) mice at different developmental and aging stages. The frequency of cobblestone area-forming cells (CAFC) day-35 in DBA fetal liver was twofold to threefold higher than in B6 mice, and by late gestation, the total stem cell number was nearly as large as that of young DBA adults. Following a further approximately 50% increase in stem cells between 6 weeks and 1 year of age, numbers in old DBA mice dropped precipitously between 12 and 20 months of age. In marked contrast, this stem cell population in B6 mice increased at a constant rate from late gestation to 20 months of age with no signs of abatement. Throughout development an inverse correlation was observed between stem cell numbers and the percentage of cells in S-phase. Because a strong genetic component contributed to the changes in stem cell numbers during aging, we quantified stem cells of 20-month old BXD recombinant inbred (RI) mice, derived from B6 and DBA progenitor strains, thus permitting detailed interstrain genetic analysis. For each BXD strain we calculated the stem cell increase or decrease as mice aged from 2 to 20 months. Net changes in CAFC-day 35 numbers among BXD strains ranged from an approximately 10-fold decrease to an approximately 10-fold increase. A genome-wide search for loci associated with this quantitative trait was performed. Several loci contribute to the trait-putative loci map to chromosomes X, 2, and 14. We conclude that stem cell numbers fluctuate widely during aging and that this has a strong genetic basis.	de Haan G, Van Zant G	Dynamic changes in mouse hematopoietic stem cell numbers during aging.	Blood	93(10)	3294-3301	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10233881&dopt=Abstract	10233881	99252083	05	2-20 months	61	610	Female	3-8	%	190		75		103						420				190		50		130				130		800		108		130		110		125						110		108		240		125		110		20		135		80		102																								6/9/2003	Mk Sullivan											10233881.05
Circadian Period		Many genes support the manifestation of the circadian period in mice. In a multiple-gene trait all genes contributing in a minor way to this characteristic are quantitative trait loci (QTL). Screens of both the BXD and the CXB panels of recombinant inbred mice suggested that distal chromosome 1, between 90 and 100 cM, contained a QTL, Cplaq3, for a difference in the circadian period of locomotor activity between the C57BL/6J and the DBA/2J and between the BALB/cBy and the C57BL/6By progenitor strains. The mice studied were a commercially available congenic strain, B6.D2-Mtv7a/Ty, from 50 to 100 days old. This congenic strain contains a small DBA/2J genomic insert that covers the region of the provisional QTL in a 99.9% C57BL/6J background. The congenic mice had a shorter period than C57BL/6J mice, confirming that this region has a QTL for the difference in period between the C57BL/6J and the DBA/2J strains. In addition, these data suggest that this region has a QTL for the mean amount of daily activity and for the pattern of locomotor activity.	Mayeda AR,        Hofstetter JR	A QTL for the genetic variance in free-running period and level of locomotor activity between inbred strains of mice.	Behav Genet	29(3)	171-176	May	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10547923&dopt=Abstract	10547923	20015646	01	100 days	100																																																																																			6/6/2002												10547923.01
Climbing scores after 16 mg/kg i.p. methamphetamine injection [quadrant crossings/min]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains.	J Neurosci	17(2)	745-754	Jan	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	10	10-14 wks	70	98	MF	8	quadrant crossings/min	2.3	0.22	0.6	0.28	0.1	0.45	-0.8	0.31	1.5	0.39	-0.8	0.38	0.3	0.32			-0.1	0.21	0.7	0.47	2.6	0.30	-1	0.48	-0.7	0.23	2	0.43	-0.3	0.29	0.4	0.39			0.1	0.17	3.3	0.21	0.7	0.39	0.8	0.51	0.6	0.35	0.6	0.38	1	0.40	-1.4	0.30	2.6	0.14	-0.8	0.48	1.6	0.34																							6/4/2003	MK Sullivan											8987796.1
Response to contextual fear [% freezing]		Fear conditioning shows associations formed between contextual or auditory stimuli with an unconditioned stimulus. Inbred mouse strains differ in their ability to demonstrate fear conditioning, suggesting at least a partial genetic influence. The present study identified the possible chromosomal loci regulating fear conditioning in BXD recombinant inbred strains using quantitative trait loci (QTL) analysis. Estimates of heritability for all 3 measures of conditioning were about .28. Correlational analyses between genetic markers and strain means identified multiple putative QTLs. The strongest associations were on Chromosomes 1 and 17 for freezing to the context, Chromosome 12 for freezing to an altered context, and Chromosome 1 for freezing to the auditory stimulus. Overlapping QTLs may indicate some common genes that underlie aspects of this learning task.	Owen EH, Christensen SC, Paylor R, Wehner JM	Identification of quantitative trait loci involved in contextual and auditory-cued fear conditioning in BXD recombinant inbred strains.	Behav Neurosci 	111(2)	292-300	Apr	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9106670&dopt=Abstract	9106670	97260550	02	60-134 days 	60	134	MF	9-20	% freezing	38	0.431	15	0.238	23	5.38	23	5.00			10	1.85	29	10.62	10	2.54	38	5.77	10	2.69	38	5.08	10	2.38			23	5.00			11	3.77			23	5.08	35	3.46	50	4.77	20	3.00	15	3.83	40	3.08	38	3.00	5	1.77	23	2.77			45	5.00																							6/12/2003	MK Sullivan											9106670.02
Decrease in body temp after TNF injection [degree C]		Administration of recombinant murine tumor necrosis factor (TNF) to mice results in lethal shock, characterized by hypotension, hypothermia, and dramatic induction of cytokines released in the circulation, such as interleukin-6 (IL-6). The sensitivity of mice to the effects of murine TNF varies from strain to strain. DBA/2 mice were found to be considerably more resistant to TNF than C57BL/6 mice. The resistance proved to be dominant since (C57BL/6 x DBA/2)F1 mice were also resistant. Using BXD recombinant inbred mice and a dose of TNF lethal for C57BL/6 but not for DBA/2 mice, we found that the resistance to TNF links to loci coding for corticosteroid-binding globulin (Cbg), alpha1-protease inhibitor (Spi1), contrapsin (Spi2) and the contrapsin-regulating gene Spi2r that form a gene cluster on chromosome 12. Quantitative trait-loci analysis of TNF-induced induction of IL-6 and of hypothermia also points to the importance of this locus (P < 0.0002 and P = 0.017, respectively), more particularly the Cbg and Spi2 loci, in the resistance to TNF. We propose to name the locus "TNF protection locus." The data suggest that endogenous protease inhibitors and/or glucocorticoids play a significant role in the attenuation of TNF-induced lethal shock. This study also demonstrates that loci affecting important biological responses can be identified with very high resolution using recombinant inbred mice.	Libert C,ÊWielockx B, Hammond GL,Ê Brouckaert P,ÊFiers W,ÊElliott RW.	Identification of a locus on distal mouse chromosome 12 that controls resistance to tumor necrosis factor-induced lethal shock.	Genomics	55(3)	284-289	Feb	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10049582&dopt=Abstract	10049582	99168897	01	15 wks	105		Female	2-9	degree C	26.3	2.21	35.1	0.27	30.1	0.59	26.2	1.69			35.4	0.15	35.5	0.18	31.9	0.63	35.6	0.11					31.3	0.94	33.3	0.96	34.5	0.31					23.6	0.58	31.6	0.75	30.4	0.84	30.2	0.25	35.6	0.16	35.4	0.23	31.2	0.56	31.6	0.12			27.2	0.49	26	1.20	34.2	0.78																					35.7	0.15	6/9/2003	MK Sullivan											10049582.01
Pentylenetetrazol (PTZ) induced seizure thresholds [mg/kg]		Gene mapping of the newly discovered SEZ genes (seizure-related genes) in the mouse was performed by linkage analysis. SEZ6 was on chromosome 11, SEZ12 on chromosome 16, SEZ15 on chromosome 3 and SEZ17 (PTZ17) on chromosome 18. The mouse chromosomal locus related to high susceptibility to pentylenetetrazol (PTZ) was also determined by linkage analysis using the recombinant inbred mouse, BXD (C57BLxDBA). A significant level of PTZ susceptibility was found on chromosome 2. Chromosomal loci of the newly discovered SEZ genes were not coincident with the significant chromosomal loci to PTZ susceptibility. Since epilepsy is assumed to be a disease syndrome which is probably manifested by abnormal expression of multifocal genes, determination of the role of each chromosomal locus in the provocation of seizure activity is important.	Wakana S, Sugaya E, Naramoto F, Yokote N, Maruyama C, Jin W, Ohguchi H, Tsuda T, Sugaya A, Kajiwara K.	Gene mapping of SEZ group genes and determination of pentylenetetrazol susceptible quantitative trait loci in the mouse chromosome.	Brain Res	857(1-2)	286-290	Feb	2000		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10700579&dopt=Abstract	10700579		01						mg/kg	35	7.1	23	2.5	30	4.2	41	4.3	28	2.7	40	7.9			25	2.5	37	2.9	32	4.7	28	3.0	27	3.9			33	2.4	31	1.5	30	0.0			29	6.4	29	3.4	29	3.4	28	2.4	29	3.4			32	5.2	34	2.8	38	4.5	33	3.2	27	3.3																							6/6/2002		Nathan Copeland										10700579.01
Imprinting - egg modifier phenotypes [% androgen development]		It is now well established that genomic imprinting effects in mammals require a combination of epigenetic modifications imposed during gametogenesis and additional modifications imposed after fertilization. The earliest post-fertilization modifications to be imposed on the genome are those thought to be mediated by factors in the egg cytoplasm. Strain-dependent differences in the actions of these egg modifiers in mice reveal an important potential for genetic variability in the imprinting process, and also provide valuable genetic systems with which to identify some of the factors that participate in imprinting. Previous studies documented a strain-dependent difference in the modification of paternal genome function between the C57BL/6 and DBA/2 mouse strains. This difference is revealed as a difference in developmental potential of androgenetic embryos produced with eggs from females of the two strains by nuclear transplantation. The specificity of the effect for the paternal genome is consistent with an effect on imprinted genes. The egg phenotype is largely independent of the genotype of the fertilizing sperm, and the C57BL/6 phenotype is dominant in reciprocal F1 hybrids. Genetic studies demonstrated that the difference in egg phenotypes between the two strains is most likely controlled by two independently segregating loci. We now report the results of experiments in which the egg phenotypes of the available BxD recombinant inbred mouse strains have been determined. The results of the analysis are consistent with the two locus model, and we have identified candidate chromosomal locations for the two loci. These data demonstrate clearly that differences in how the egg cytoplasm modifies the incoming paternal genome are indeed genetically determined, and vary accordingly.	Latham KE, Sapienza C.	Localization of genes encoding egg modifiers of paternal genome function to mouse chromosomes one and two.	Development 	125(5)	929-935	Mar	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9449675&dopt=Abstract	9449675		01				Female		%					41		56		23		52		41		50		57		8				46		39		62		71		32		27		10		61		51		46		64		61		44		20		64		49		63																								6/6/2002		Nathan Copeland										9449675.01
Ethanol induced locomotor response distance traveled, 0-5 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	06	8-12wks	56	84	Male	4-18	cm	208	321	2284	261	1274	516			323	413	-208	364	1182	324	289	370	308	265	1819	347	925	291	146	375	943	341	1845	410	2042	447	1786	338	1423	389	1228	250	481	269	109	420	683	560	698	403	447	266	486	126	155	600	983	495	414	325	1073	289																							6/6/2003	MK Sullivan		ETBethanol									9880575.06
Ethanol induced locomotor response distance traveled, 5-10 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	07	8-12wks	56	84	Male	4-18	cm	536	330	1689	353	533	283			-144	293	-504	420	1387	322	-2024	460	459	213	2298	279	392	306	288	224	-119	132	1884	351	2243	436	264	402	2291	437	1904	361	-1116	257	-138	318	-281	444	-378	558	1689	528	566	142	1038	253	902	424	671	216	515	296																							6/6/2003	MK Sullivan		ETBethanol									9880575.07
Ethanol induced locomotor response distance traveled, 10-15 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	08	8-12wks	56	84	Male	4-18	cm	356	331	1094	233	182	265			-824	280	-1115	348	1344	318	-2458	169	599	249	1244	141	282	199	-354	416	-324	158	1555	427	2235	367	-357	444	1742	498	1693	339	-591	233	-450	260	-319	336	-634	355	800	368	749	203	799	325	758	315	908	301	766	391																							6/6/2003	MK Sullivan		ETBethanol									9880575.08
Ethanol induced locomotor response distance traveled, 15-20 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	09	8-12wks	56	84	Male	4-18	cm	215	232	739	207	639	336			-936	270	-1376	316	1147	309	-2107	151	578	280	1495	188	-308	296	-857	304	-420	133	1416	422	1799	299	-606	424	1234	241	1406	323	-528	233	-173	248	-380	293	-711	375	319	396	515	269	142	369	1065	211	1225	200	851	238																							6/6/2003	MK Sullivan		ETBethanol									9880575.09
Ethanol induced locomotor response distance traveled, 5-20 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	10	8-12wks	56	84	Male	4-18	cm	1107	893	3522	793	1354	884			-1905	843	-2995	1083	3879	950	-6588	779	1636	743	5037	608	366	800	-923	944	-864	423	4855	1200	6277	1102	-717	1271	5267	1175	5003	1023	-2235	724	-761	826	-979	1073	-1722	1288	2808	1293	1829	614	1980	947	2725	951	2805	716	2132	924																							6/6/2003	MK Sullivan		ETBethanol									9880575.1
Eye weight [mg] [strains 33 to 42 calculated 6/28/00]		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	03	106 days	106		MF	8-35	mg	18.9	0.2	20.2	0.2	20.1	0.4	20.1	0.2	19.6	0.3	19.7	0.3	18.7	0.3	19.4	0.3	20.3	0.3	18.9	0.2	18.2	0.3	18.3	0.2	19.1	0.3	19.3	0.1	17.3	0.4	20.1	0.2	19.4	0.2	15.6	0.4	19.3	0.2	18.4	0.2	16.3	0.3	16.8	0.3	19.2	0.2	17.5	0.2	19.4	0.3	17.8	0.5	20	0.3	20	0.3	F										19.5												6/12/2003	MK Sullivan											10102277.03
Forebrain weight [mg] [raw average from strainDB 6/28/00]			Williams RW unpub		unpublished				2000					82	100 days	100		MF		mg																	300.8		295.4		288.4		311.1		323.4		331.2		316.3				275.0		323.9		322.8		288.5		295.2		286.3		260.9		282.7		277.9		257.2		293.4		311.2																								12/19/2002												.82
Ethanol induced conditioned place preference - Grid floor preference after 2 g/kg ethanol i.p. paired with grid [s/min]	table 3 col 1	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	10	56-125 days	56	125	Male	6-17	s/min	35.6	1.9	36.0	2.5	43.7	2.8	40.9	2.0	32.1	2.3	38.6	2.5	36.2	2.0	36.1	2.5	50.5	2.9	35.7	2.5	33.7	2.8	35.7	2.1	36.1	2.9	40.5	5.0	34.5	1.7					31	1.7	36.3	4.9			45.7	2.9	33.8	1.7	43.5	3.0	31.2	2.9	34.5	1.5																													6/23/2003	MK Sullivan											7480533.1
Ethanol induced conditioned place preference - Hole floor preference after 2 g/kg ethanol i.p. paired with hole floor [s/min]	table 3 col 2	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	11	56-125 days	56	125	Male	7-17	s/min	25.6	2.3	24.4	3.5	26.0	2.9	25.8	3.7	26.6	2.5	22.8	2.5	22.5	2.0	24.0	1.9	16.0	3.3	26.1	2.8	22.1	2.0	29.4	2.4	19.4	2.2	26.4	4.0	253	2.0					31.5	1.7	17.4	3.8			16.2	3.1	33.7	1.8	23.0	3.9	25.7	3.2	30.5	1.8																													6/23/2003	MK Sullivan											7480533.11
High Affinity Choline Uptake (concentration of 0.5*10^-6M) in frontal cortex [pmole/4min/mg protein]		Using the quantitative trait loci (QTL) approach, preliminary identification has been made of a region on mouse chromosome 17 that influences high-affinity choline uptake (HACU) in the mouse brain. The rate of HACU was measured in synaptosomes prepared from the frontal cortex, hippocampus, and striatum of C57BL/6J (B6), DBA/2J (D2), and 25 BXD recombinant inbred (RI) strains of mice, using a final concentration of 0.5 microM [3H]choline. The strain means of HACU in each area were then correlated with the strain distribution pattern of each of 1300 known genetic markers using a point biserial correlation and 0 (B6 allele) and 1 (D2 allele). Correlations of P < 0.00001 were found between striatal HACU and chromosome 17 markers D17Tu50 and Tcp1. Correlations of P < 0.0001 were found between striatal HACU and chromosome 17 markers D17Leh66e, D17Leh119, D17Rp17e, Plg, D17Leh66d, Ckb-rs2, and Trp53-ps. QTL analyses of HACU in the frontal cortex and hippocampus also revealed correlations with these markers at the level of P < 0.05 and P < 0.01. These data suggest that at least one locus located on mouse chromosome 17 near or between 6 and 13 cM from the centromere influences HACU in the striatum and possibly the frontal cortex and hippocampus of the mouse.	Tarricone BJ, Hwang WG, Hingtgen JN, Mitchell SR, Belknap JK, Nurnberger JI	Identification of a locus on mouse chromosome 17 associated with high-affinity choline uptake using BXD recombinant inbred mice and quantitative trait loci analysis	Genomics	27(1)	161-164	May	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7665164&dopt=Abstract	7665164	95394453	01	12-14 wks	84	98	Male	4	pmole/4min/mg protein	17.2	1.8	13.1	1.1	18.5	1.8	17.3	2.2	13.7	1.4	15.4	0.9	25	1.3	22.1	1.5	12.8	1.9	17.8	1.7	25.5	2.6	19	5.5	24.4	2.4	17.3	2.0	18.2	2.1	24.9	3.0			23.4	3.0	16.4	1.2	26.8	4.5	19.3	4.1	23.7	2.2	17.3	2.0	21.2	0.4	20.5	1.9	18.7	1.2	12.5	2.0	25.9	1.7																							6/11/2003	MK Sullivan											7665164.01
High Affinity Choline Uptake (concentration of 0.5*10^-6M) in hippocampus [pmole/4min/mg protein]		Using the quantitative trait loci (QTL) approach, preliminary identification has been made of a region on mouse chromosome 17 that influences high-affinity choline uptake (HACU) in the mouse brain. The rate of HACU was measured in synaptosomes prepared from the frontal cortex, hippocampus, and striatum of C57BL/6J (B6), DBA/2J (D2), and 25 BXD recombinant inbred (RI) strains of mice, using a final concentration of 0.5 microM [3H]choline. The strain means of HACU in each area were then correlated with the strain distribution pattern of each of 1300 known genetic markers using a point biserial correlation and 0 (B6 allele) and 1 (D2 allele). Correlations of P < 0.00001 were found between striatal HACU and chromosome 17 markers D17Tu50 and Tcp1. Correlations of P < 0.0001 were found between striatal HACU and chromosome 17 markers D17Leh66e, D17Leh119, D17Rp17e, Plg, D17Leh66d, Ckb-rs2, and Trp53-ps. QTL analyses of HACU in the frontal cortex and hippocampus also revealed correlations with these markers at the level of P < 0.05 and P < 0.01. These data suggest that at least one locus located on mouse chromosome 17 near or between 6 and 13 cM from the centromere influences HACU in the striatum and possibly the frontal cortex and hippocampus of the mouse.	Tarricone BJ, Hwang WG, Hingtgen JN, Mitchell SR, Belknap JK, Nurnberger JI	Identification of a locus on mouse chromosome 17 associated with high-affinity choline uptake using BXD recombinant inbred mice and quantitative trait loci analysis	Genomics	27(1)	161-164	May	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7665164&dopt=Abstract	7665164	95394453	02	12-14 wks	84	98	Male	4	pmole/4min/mg protein	17.5	1.5	14.2	1.2	17.6	1.6	18.9	1.7	22.4	1.5	18.9	1.4	20.8	3.4	25.9	2.4	21.2	2.3	19.9	0.9	27.7	4.0	22.2	1.5	23.3	2.4	17.4	1.4	19.1	1.4	28.5	2.7			25.2	3.3	21.6	1.8	26.2	3.2	17.9	2.6	36	3.0	21	2.6	22.4	1.2	30.3	3.4	22.8	1.6	17.7	5.7	23.6	4.8																							6/11/2003	MK Sullivan											7665164.02
High Affinity Choline Uptake (concentration of 0.5*10^-6M) in striatum [pmole/4min/mg protein]		Using the quantitative trait loci (QTL) approach, preliminary identification has been made of a region on mouse chromosome 17 that influences high-affinity choline uptake (HACU) in the mouse brain. The rate of HACU was measured in synaptosomes prepared from the frontal cortex, hippocampus, and striatum of C57BL/6J (B6), DBA/2J (D2), and 25 BXD recombinant inbred (RI) strains of mice, using a final concentration of 0.5 microM [3H]choline. The strain means of HACU in each area were then correlated with the strain distribution pattern of each of 1300 known genetic markers using a point biserial correlation and 0 (B6 allele) and 1 (D2 allele). Correlations of P < 0.00001 were found between striatal HACU and chromosome 17 markers D17Tu50 and Tcp1. Correlations of P < 0.0001 were found between striatal HACU and chromosome 17 markers D17Leh66e, D17Leh119, D17Rp17e, Plg, D17Leh66d, Ckb-rs2, and Trp53-ps. QTL analyses of HACU in the frontal cortex and hippocampus also revealed correlations with these markers at the level of P < 0.05 and P < 0.01. These data suggest that at least one locus located on mouse chromosome 17 near or between 6 and 13 cM from the centromere influences HACU in the striatum and possibly the frontal cortex and hippocampus of the mouse.	Tarricone BJ, Hwang WG, Hingtgen JN, Mitchell SR, Belknap JK, Nurnberger JI	Identification of a locus on mouse chromosome 17 associated with high-affinity choline uptake using BXD recombinant inbred mice and quantitative trait loci analysis	Genomics	27(1)	161-164	May	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7665164&dopt=Abstract	7665164	95394453	03	12-14 wks	84	98	Male	4	pmole/4min/mg protein	80.1	5.7	64.8	5.9	52.4	4.6	62.8	7.0	43.5	4.0	55.5	8.0	112.1	13.9	94.2	14.4	59.4	6.6	54.7	7.2	92.3	23.3	90.4	13.6	112.8	10.0	62.7	2.2	55.2	4.7	107.1	11.3			89.3	7.8	59.5	4.2	107.9	10.2	51.7	3.4	128.9	4.8	76.2	4.7	78.1	4.1	79.2	7.6	51.6	3.2	52.5	4.1	87.2	9.6																							6/11/2003	MK Sullivan											7665164.03
Haloperidol induced catalepsy - ED50 [mg/kg]		The strain means for haloperidol-induced catalepsy were determined in the 26 strain BXD recombinant inbred series. The ED50 values ranged from 0.55 mg/kg (strain 30) to 7.9 mg/kg (strain 2). Heritability for the catalepsy response was 0.78 and the number of effective loci was estimated to be four. The strain means were correlated with the strain distribution patterns for 1300 marker loci of known chromosomal location and polymorphic between the C57Bl/6J and DBA/2J strains. Six quantitative trait loci (QTLs) were identified at P < .01. Two of the six QTLs were confirmed in a sample of B6XD2 F2 animals (n = 144), phenotyped for haloperidol response and genotyped for microsatellites closely linked to the QTLs. The confirmed QTL on chromosome 4 is near the b locus. The confirmed QTL on chromosome 9 is closely linked to Drd2, the D2 dopamine receptor gene. One hundred of the F2 individuals were phenotyped for D2 dopamine receptor binding using the ligand [125I] epidepride as the ligand. Consistent with previous results, the nonresponsive F2 individuals showed modestly higher receptor binding in all brain regions examined: the nucleus accumbens core, the nucleus accumbens shell, the lateral caudate putamen, the dorsomedial caudate putamen, the substantia nigra zona compacta and the ventral tegmental area. The DBA/2J allele of the chromosome 9 QTL was associated with higher receptor binding in all brain areas except the ventral tegmental area. Overall, the data illustrate that either near or part of Drd2 is a QTL which has significant effects on both haloperidol response and D2 dopamine receptor binding. However, the data also illustrate that most of the genetic variance in either haloperidol response or D2 dopamine receptor binding is not associated with Drd2.	Kanes S, Dains K	Mapping the genes for haloperidol-induced catalepsy.	J Pharmacol Exp Ther	277(2)	1016-1025	May	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627512&dopt=Abstract	8627512	96210104	01	100 days	100		MF		mg/kg	3.8		0.4		1.17		7.9		1.23		3.25		1.48		1.73		2.47		2.94		1.53		2.31		1.17		4.18		4.43		2.39		2.8		0.98		0.61		5.89		0.93		3.62		1.35		2.73		6.67		0.55		0.96		3.81																								6/6/2002												8627512.01
High Dose Sensitivity to ethanol sleep time female [min]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	05	117-137 days	117	137	Female	7-15	min	103.83		116.46		109.89		121.93		17.96		112.66		125.27		97.84		107.41		159.76		91.98		119.62				104.52								100.89		132.81				110.6		115.38		111.68		116.27		119.97				146.8		141.16																								7/11/2003	MK Sullivan											7695038.05
High Dose Sensitivity to ethanol sleep time male [min]		Although the recombinant inbred strain method was designed for molecular genetic analysis of linkage, it also provides powerful quantitative genetic analyses of heritability and genetic correlations. Measures of alcohol acceptance, alcohol preference, and hypnotic dose sensitivity (HDS) were assessed in 21 strains of mice from the BXD RI series. Sex differences were found to be significant at a phenotypic level. However, heritability estimates for acceptance, preference, and HDS are similar in males and females. Heritability estimates for the three measures are approximately 0.20 for acceptance and preference, and 0.10 for HDS. Analyses of genetic correlations reveal that acceptance and preference share some degree of genetic influence, although they mostly operate under different genetically mediated mechanisms. HDS did not show a significant genetic relationship to either acceptance or preference. Strong correlations were obtained when acceptance, preference, and HDS strain means were correlated across male and female recombinant inbreds, suggesting substantial genetic similarity across sexes.	Rodriguez LA, Plomin R, Blizard DA, Jones BC, McClearn GE	Alcohol acceptance, preference, and sensitivity in mice. I. Quantitative genetic analysis using BXD recombinant inbred strains	Alcohol Clin Exp Res	18(6)	1416-1422	Dec	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7695038&dopt=Abstract	7695038	95209059	06	117-137 days	117	137	Male	7-17	min	118.43		108.61		116.96		142.79		150.8		136.34		126.14		109.79		109.32		157.56		125		105.96				140.48								103.54		153.76				129.67		145.67		128.02		109.74		128.2				141.96		154.62																								7/11/2003	MK Sullivan											7695038.06
High Dose Sensitivity to ethanol - Duration (mins) of loss of righting reflex following 4.1 g/kg EtOH i.p.		Quantitative trait loci (QTL) mapping of complex phenotypes has emerged as an important feature of the recombinant inbred (RI) strain methodology. In this second study of our series on alcohol-related behaviors in mice, we examine alcohol acceptance, preference, and hypnotic dose sensitivity (HDS) to a standard dose of alcohol measured in BXD RI strains to identify candidate QTL regions responsible for their heritability. We detected highly significant marker associations for acceptance on chromosome 12 (Eif4e), for preference on chromosome 1 (D1Rti2) and chromosome 7 (D7Mit7), and for HDS on chromosome 7 (Mpmv1). These are the strongest QTL associations that we detected, but several other candidate QTL regions are reported. Given the limited number of BXD RI strains available, the large number of markers used herein, and the consequent chance of identifying false marker associations, these RI QTL mapping results must be seen as tentative, but an important first step toward identifying QTL for alcohol-related behaviors.	Rodriguez LA,Ê Plomin R,ÊBlizard DA, Jones BC,Ê McClearn GE.	Alcohol acceptance, preference, and sensitivity in mice. II. Quantitative trait loci mapping analysis using BXD recombinant inbred strains	Alcohol Clin Exp Res	19(2)	367-373	Apr	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7625571&dopt=Abstract	7625571	95351511	03	117-137days	117	137	MF	15-31	min	112.1		112.41		113.21		132.36		139.98		124.5		125.7		103.5		108.37		158.71		110.55		112.39				118.9								102.21		144.6				120.13		127.85		119.85		113		124.08				144.54		148.24																								7/11/2003	MK Sullivan		ETCONS10(PSU)	HDS	HDS           High Dose Sensitivity	EtOH	4.1 g/kg		Rodriguez	p. 369, Table 1	MRG 120601 from publication	7625571.03
Hemopoietic stem cell cycling day 7 [% CAFC]		Normal somatic cells undergo replicative senescence in vitro but the significance of this process in organismic aging remains controversial. We have shown previously that hemopoietic stem cells of common inbred strains of mice vary widely in cycling activity and that this parameter is inversely correlated with strain-dependent mean life span. To assess whether cell cycling and life span are causally related, we searched for quantitative trait loci (QTLs) that contributed to variation of these traits in BXH and BXD recombinant inbred mice. Two QTLs, mapping to exactly the same intervals on chromosomes 7 and 11, were identified that were associated with variation of both cell cycling and life span. The locus on chromosome 11 mapped to the cytokine cluster, a segment that shows synteny with human chromosome 5q, in which deletions are strongly associated with myelodysplastic syndrome. These data indicate that steady-state cell turn-over, here measured in hemopoietic progenitor cells, may have a significant effect on the mean life span of mammals.	de Haan G, Van Zant G                                                                                                                                                                                                                                                                                                                                                                                                              	Genetic analysis of hemopoietic cell cycling in mice suggests its involvement in organismal life span.	FASEB J	13(6)	707-713	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10094931&dopt=Abstract	10094931	99196952	01	6-8 wks	42	56	Female	10-20	%	8	10.4	20	9.8	36	10.6	12.6	11.1	31	9.7	31	7.8	13	10.8	2	7.6	29	7.6	16	8.3	26	6.3	18	8.9	22	9.0	34	8.6	13	6.1	2	11.5	0.8	11.2	32	9.6	6	6.8	12.6	12.0	7.8	12.8	0.8	7.6	12.8	11.1	24	8.7	19	6.1	0.8	9.4	56	3.3	34	8.9																							6/9/2003	MK Sullivan											10094931.01
Hindbrain weight [mg] [raw average from strainDB 6/28/00]			Williams RW unpub		unpublished				2000					81	100 days	100		MF		mg																	42.5		46.5		42.0		43.4		39.1		44.1		44.7		43.1		34.3		36.2		42.6		41.8		46.3		39.2		30.8		44.4		41.5		38.6		43.6		50.1																								12/19/2002												.81
Hippocampus weight [raw average from strainDB 6/28/00]		Notable differences in hippocampal structure are associated with intriguing differences in development and behavioral capabilities. We explored genetic and environmental factors that modulate hippocampal size, structure, and cell number using sets of C57BL/6J (B6) and DBA/2J (D2) mice; their F1 and F2 intercrosses (n = 180); and 35 lines of BXD recombinant inbred (RI) strains. Hippocampal weights of the parental strains differ by 20%. Estimates of granule cell number also differ by approximately 20%. Hippocampal weights of RI strains range from 21 to 31 mg, and those of individual F2 mice range from 23 to 36 mg (bilateral weights). Volume and granule cell number are well correlated (r = 0.7-0.8). Significant variation is associated with differences in age and sex. The hippocampus increases in weight by 0.24 mg per month, and those of males are 0.55 mg heavier (bilateral) than those of females. Heritability of variation is approximately 50%, and half of this genetic variation is generated by two quantitative trait loci that map to chromosome 1 (Hipp1a: genome-wide p < 0.005, between 65 and 100 cM) and to chromosome 5 (Hipp5a, p < 0.05, between 15 and 40 cM). These are among the first gene loci known to produce normal variation in forebrain structure. Hipp1a and Hipp5a individually modulate hippocampal weight by 1.0-2.0 mg, an effect size greater than that generated by age or sex. The Hipp gene loci modulate neuron number in the dentate gyrus, collectively shifting the population up or down by as much as 200,000 cells. Candidate genes for the Hipp loci include Rxrg and Fgfr3.	Lu L, Airey DC, Williams RW	Complex trait analysis of the hippocampus: mapping and biometric analysis of two novel gene loci with specific effects on hippocampal structure in mice.	J Neurosci	21(10)	3503-3514	May	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331379&dopt=Abstract	11331379		01	100 days	100		MF							27.1		25.3		26.8		26.3		26.2		25.4		25.5		26.4		24.7		26.0		27.9		28.3		26.2		28.3		24.3		26.5		25.3		24.3		23.9		24.5		23.3		23.1		22.1		21.1		23.6		25.3		26.3		23.8		26.1		25.7		24.5		27.3		24.7		30.5				27.4				12/20/2002												11331379.01
Induction of serum IL-6 after TNF injection [ng/ml]		Administration of recombinant murine tumor necrosis factor (TNF) to mice results in lethal shock, characterized by hypotension, hypothermia, and dramatic induction of cytokines released in the circulation, such as interleukin-6 (IL-6). The sensitivity of mice to the effects of murine TNF varies from strain to strain. DBA/2 mice were found to be considerably more resistant to TNF than C57BL/6 mice. The resistance proved to be dominant since (C57BL/6 x DBA/2)F1 mice were also resistant. Using BXD recombinant inbred mice and a dose of TNF lethal for C57BL/6 but not for DBA/2 mice, we found that the resistance to TNF links to loci coding for corticosteroid-binding globulin (Cbg), alpha1-protease inhibitor (Spi1), contrapsin (Spi2) and the contrapsin-regulating gene Spi2r that form a gene cluster on chromosome 12. Quantitative trait-loci analysis of TNF-induced induction of IL-6 and of hypothermia also points to the importance of this locus (P < 0.0002 and P = 0.017, respectively), more particularly the Cbg and Spi2 loci, in the resistance to TNF. We propose to name the locus "TNF protection locus." The data suggest that endogenous protease inhibitors and/or glucocorticoids play a significant role in the attenuation of TNF-induced lethal shock. This study also demonstrates that loci affecting important biological responses can be identified with very high resolution using recombinant inbred mice.	Libert C,ÊWielockx B, Hammond GL,Ê Brouckaert P,ÊFiers W,ÊElliott RW.	Identification of a locus on distal mouse chromosome 12 that controls resistance to tumor necrosis factor-induced lethal shock.	Genomics	55(3)	284-289	Feb	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10049582&dopt=Abstract	10049582	99168897	02	15 wks	105		Female	2-9	ng/ml	5	0.49	2.45	0.12	4	0.20	5.3	0.42			2.5	0.34	3	0.17	2.9	0.40	2.5	0.19					5.5	0.21	2.95	0.14	2.55	0.40					4.4	0.23	4.25	0.15	4.8	0.28	5	0.40	1.8	0.03	2.5	0.12	2.8	0.10	3	0.50			4.3	0.33	4.9	0.45	1.7	0.07																					2.2	0.10	6/9/2003	MK Sullivan											10049582.02
Prepulse Inhibition of the Acoustic Startle Response to 110 dB SPL white-noise bursts, 5 kHz, 80 dB Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	08	100 days	100		MF	9-15	%	50.8		24.4		31.6				34.8		17.5		36.3		40.7		9.9				35.3		-6.7		14.2		12.3				34.1						16		39.5		-14.6		19		11.6		19		31.5		-9.9		14.9		-10.4																								12/27/2002	Ryan McNeive	Ryan McNeive										10371755.08
Prepulse Inhibition of the Acoustic Startle Response to 110 dB SPL white-noise bursts, 10 kHz,80 dB Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	09	100 days	100		MF	9-15	%	62.9		42.2		46.6				40.2		15.8		45.9		49.3		38				37.8		12.5		17.4		6.2				43.1						16.7		24.8		-2.7		27.4		20.6		39.1		37.5		-1		19.8		4.2																								12/27/2002	Ryan McNeive	Ryan McNeive										10371755.09
Prepulse Inhibition of the Acoustic Startle Response to 110 dB SPL white-noise bursts, 15 kHz, 80 dB Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	10	100 days	100		MF	9-15	%	46		45.9		40.8				54.7		25.5		27		37.5		33.3				25.6		-1.9		-10.6		6.6				22.4						15.6		59.4		17.1		41		4.5		29.8		46.2		14.8		18.8		-6.6																								12/27/2002	Ryan McNeive	Ryan McNeive										10371755.1
Prepulse Inhibition of the Acoustic Startle Response to 110 dB SPL white-noise bursts, 20 kHz, 80 dB Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	11	100 days	100		MF	9-15	%	40.6		9.2		31.6				23		15.3		13.6		21.7		25.7				11.8		-9.7		8.8		-7.3				7.1						9.6		31.9		-6.3		0.2		2.7		13.2		32.2		-2.6		13.1		-3.4																								12/27/2002	Ryan McNeive	Ryan McNeive										10371755.11
Prepulse Inhibition of the Acoustic Startle Response to a 110-db SPL, 10 kHz tone, 56-db SPL white-noise Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	12	100 days	100		MF	9-15	%	26.8		2.1		44				25.9		13.4		60.1		35.7		13.3		35.4		30.4		27.9		13.7		9.8		59.5		8.4				44.7		36.2				15.1		39.1		4.9		25.1		3.4		35.8		15.2		17.8																								12/27/2002	Ryan McNeive	Ryan McNeive										10371755.12
Prepulse Inhibition of the Acoustic Startle Response to a 110-db SPL, 10 kHz tone, 68-db SPL white-noise Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	13	100 days	100		MF	9-15	%	32.8		15.5		53				30.5		15.2		65.3		31.5		14.2		21.4		35.2		33.8		18.1		12.9		57.9		28.4				40.6		51				24.2		39.8		13		38		18.3		38.6		28.5		25.8																								6/6/2002	Ryan McNeive	Ryan McNeive										10371755.13
Prepulse Inhibition of the Acoustic Startle Response to a 110-db SPL, 10 kHz tone, 80-db SPL white-noise Prepulse Stimulus [%] 		The measurement of the acoustic startle response (ASR) and prepulse inhibition (PPI) of the ASR in many inbred strains of mice, including C57BL/6 and DBA/2, may be complicated by age-related high-frequency hearing loss (HFHL) and the associated cochlear pathology. Willott and Erway (1998) have recently reported on the age-related changes of the acoustic brain response in the BXD recombinant inbred (RI) series. Based on these data, the RI series was divided into three groups: juvenile-, intermediate-, and adult-onset HFHL. Each of these groups was tested using paradigms which varied the frequency or intensity of the auditory startle and prepulse stimuli. The results obtained in adolescent mice (6-8 weeks) demonstrate that ASR performance is independent of HFHL; there was no group-dependent decline in the ASR amplitudes for high-frequency stimuli. The expected effect of HFHL on PPI is to increase the salience of the still-audible tones. In response to a white-noise prepulse stimulus, the PPI in the juvenile-onset group (which shows marked HFHL at 6 weeks) was similar to that in the adult-onset group. However, when the prepulse stimulus was a pure tone, the juvenile group showed a decrease in salience across all frequencies tested (5-20 kHz). The data point out the need for carefully constructing auditory tasks in the BXD RI series, to avoid the confounding effects of HFHL.	McCaughran J, Bell J, Hitzemann R	On the relationships of high-frequency hearing loss and cochlear pathology to the acoustic startle response (ASR) and prepulse inhibition of the ASR in the BXD recombinant inbred series	Behav Genet	29(1)	21-30	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371755&dopt=Abstract	10371755	99300343	14	100 days	100		MF	9-15	%	42.9		22.6		62.4				29.4		30.1		75.1		33.4		35.9		32.8		46.2		37.5		25.6		21.8		58.5		34.4				7.9		48.7				36.4		50.6		21.7		55.6		14.2		37.5		42.3		42.9																								6/6/2002	Ryan McNeive	Ryan McNeive										10371755.14
Initial sensitivity to ethanol induced ataxia, onset threshold [mg/kg]		Rapid tolerance to rotarod ataxia has previously been demonstrated in mice after sequential ethanol injections. Here we tested DBA/2J and C57BL/6J mice for initial ethanol sensitivity; DBA/2J mice were more sensitive (0.40 +/- 0.17 mg/g brain) than C57BL/6J mice (1.44 +/- 0.12 mg/g). We then monitored the development of tolerance by quantifying blood ethanol concentrations at the recovery from ataxia over five sequential injections; tolerance reached a plateau in about 5 hr. DBA/2J mice became very tolerant (final ethanol threshold 3.47 +/- 0.16 mg/ml, an increase of 3.07 mg/ml, or 8.7-fold above base line); B6 became slightly tolerant (final ethanol threshold 2.62 +/- 12 mg/ml, and increase of 1.18, or 1.8-fold above base line). Therefore, by the end of the treatment regimen, the rank order of sensitivity of the two strains had reversed. We then tested 25 recombinant inbred strains from among strains representing a cross between C57BL/6J and DBA/2J inbred strains, followed by a quantitative trait locus analysis with a database of 1522 markers to identify provisional loci. This procedure identified 19 markers on 11 chromosomes for initial sensitivity, 18 markers on 9 chromosomes for tolerance (delta) and 21 markers on 11 chromosomes for tolerance (fold-increase). Of these, 17 markers were in common, which suggests that initial sensitivity and tolerance share substantial genetic codetermination. Major candidate loci will be confirmed by genotyping B6D2F2 offspring that have been tested for initial sensitivity and tolerance.	Gallaher EJ, Jones GE	Mapping the genes for haloperidol-induced catalepsy.	J Pharmacol Exp Ther	277(2)	604-612	May	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627537&dopt=Abstract	8627537	96210104	01	44-135 days	44	135	Male	4-16	mg/kg	1.44		0.4		1.21		1.09		0.8		1.03		0.77		1.16		0.88		0.94		0.71		0.8		0.41		1.22		1.28		0.98				1.07		0.49		0.9		0.72		1.07		0.8		0.69		1.37		1.03		1.15		0.44																								12/19/2002												8627537.01
Intensity of Immune complex deposits detected in kidneys immunized with the 16/6Id [0=no immune complexes; 1=1 - 5 immune complex deposits; 2=5 - 20 immune complaex deposits; 3=20 - 50 immune complex depostits; 4=50 immune complex depostis]		The DBA/2 and C57BL/6 mouse strains, as well as the BXD RI lines derived from these strains, were used to map the genes controlling experimentally induced systemic lupus erythematosus (SLE). SLE was induced using two immunologic approaches: (1) immunization with the human monoclonal anti-DNA antibody expressing the 16/6Id, to which the DBA/2 strain is susceptible (responder) and the C57BL/6 strain is resistant (nonresponder); and (2) induction of autoimmune GVHD in B6D2F1 hosts by inoculation of parental DBA/2 (induces SLE) or C57BL/6 (does not induce SLE) T cells. By both approaches the BXD RI lines could be divided into distinct DBA/2-like and C57BL/6-like categories. Concordance of SLE induced by both methods was observed for susceptibility and resistance in 13/15 BXD lines (P < 0.005). The results suggest that at least two non-H-2 genes control susceptibility and resistance to experimentally induced SLE, one mapping to chromosome 7 and the other mapping to chromosome 14.	Mozes E, Alling D, Miller MW, Payne SM, Zinger H, Via CS, Shearer GM.	Genetic analysis of experimentally induced lupus in mice.	Clin Immunol Immunopathol	85(1)	28-34	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9325066&dopt=Abstract	9325066		01	6-8 wks	42	56	MF	5-10	0=no immune complexes; 1=1 - 5 immune complex deposits; 2=5 - 20 immune complaex deposits; 3=20 - 50 immune complex depostits; 4=50 immune complex depostis	0		3		0		3		2		0				2		3		0		0		4		0		0		0						0		1				0		2																																				6/6/2003	MK Sullivan	Nathan Copeland										9325066.01
Lens weight [mg]		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	04	106 days	106		MF	8-35	mg	5.9		6.7		6.2		6.1		5.7		5.9		5.8		6		6		5.3		5.3		5.7		5.7		6.1		5.2		6.5		5.5		4.8		6		5.5		5.3		5.3		5.6		5		5.9		5.5		6		6.2																								6/12/2003	MK Sullivan											10102277.04
Lethality due to TNF injection [%]		Administration of recombinant murine tumor necrosis factor (TNF) to mice results in lethal shock, characterized by hypotension, hypothermia, and dramatic induction of cytokines released in the circulation, such as interleukin-6 (IL-6). The sensitivity of mice to the effects of murine TNF varies from strain to strain. DBA/2 mice were found to be considerably more resistant to TNF than C57BL/6 mice. The resistance proved to be dominant since (C57BL/6 x DBA/2)F1 mice were also resistant. Using BXD recombinant inbred mice and a dose of TNF lethal for C57BL/6 but not for DBA/2 mice, we found that the resistance to TNF links to loci coding for corticosteroid-binding globulin (Cbg), alpha1-protease inhibitor (Spi1), contrapsin (Spi2) and the contrapsin-regulating gene Spi2r that form a gene cluster on chromosome 12. Quantitative trait-loci analysis of TNF-induced induction of IL-6 and of hypothermia also points to the importance of this locus (P < 0.0002 and P = 0.017, respectively), more particularly the Cbg and Spi2 loci, in the resistance to TNF. We propose to name the locus "TNF protection locus." The data suggest that endogenous protease inhibitors and/or glucocorticoids play a significant role in the attenuation of TNF-induced lethal shock. This study also demonstrates that loci affecting important biological responses can be identified with very high resolution using recombinant inbred mice.	Libert C,ÊWielockx B, Hammond GL,Ê Brouckaert P,ÊFiers W,ÊElliott RW.	Identification of a locus on distal mouse chromosome 12 that controls resistance to tumor necrosis factor-induced lethal shock.	Genomics	55(3)	284-289	Feb	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10049582&dopt=Abstract	10049582	99168897	03	15 wks	105		Female	2-9	%	100		0		79		100		66		0		0		12		0				0		89		0		20		56		75		100		100		89		100		10		0		10		20				100		83		10																								6/9/2003	MK Sullivan											10049582.03
Locomotor activity, 1 - 5 min habituation after single saline i.p. injection (experimental group) [activity/min]	table 1 col 1	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	12	56-125 days	56	125	Male	13-34	activity counts/min	116.2	5.5	65.1	5.8	116.0	5.7	83.7	6.1	54.9	6.0	106.7	7.8	47.4	2.1	76.6	5.6	50.4	4.1	91.5	6.3	60	3.1	97.6	8.6	53	2.4	48.3	1.9	87.1	4.1					52.1	1.9	48.4	3.7			47.3	2.5	85.8	6.6	49.9	7.1	44.5	3.4	146.4	6.8																													6/23/2003	MK Sullivan											7480533.12
Locomotor activity, 1 - 5 min after saline (experimental group trial 1) [activity counts per min]	table 1 col 2	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	13	56-125 days	56	125	Male	13-34	activity counts/min	87.8	4.8	63.7	3.3	92.4	3.6	73.5	6.0	40.4	1.7	82.3	3.9	48.1	2.6	73.6	4.4	45.7	2.6	66	4.7	46.3	2.7	66.6	4.0	45.9	1.9	45.7	1.4	83.5	4.0					53.6	1.6	47	2.0			38.8	2.7	8.7	3.9	60.1	5.6	51.9	3.8	143.6	4.5																													6/23/2003	MK Sullivan			Saline: Trial 1								7480533.13
Locomotor activity, 1 - 5 min after saline i.p., trial 4 (experimental group, prior Ethanol exposure) [activity counts per min]	table 1 col 3	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	04	56-125 days	56	125	Male	13-34	activity counts/min	39.9	1.9	53.5	4.6	54.6	3.6	36.9	3.9	27.3	1.6	40.4	2.9	29.7	2.6	52.8	3.4	24.1	1.9	33.8	3.5	23.8	2.0	42.7	2.8	37.6	2.0	28.2	1.4	68.8	4.0					47.6	2.4	35.7	2.6			32.4	2.9	49.8	3.1	34	4.4	37.8	4.5	124.7	6.1																													6/23/2003	MK Sullivan			Saline: Trial 4								7480533.04
Locomotor activity, 1 - 5 min after 2 g/kg ethanol i.p. conditioning trial 1 [activity counts per min]	table 1 col 4	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	05	56-125 days	56	125	Male	13-34	2 g/kg IP, activity counts/min	116.7	8.0	138.9	8.8	134.6	9.3	93.7	4.3	76.8	2.6	97.8	4.6	134	7.1	122.6	4.4	98.1	7.2	68.1	5.2	89.4	5.9	124.6	7.5	64.1	3.8	60.7	3.4	128.0	6.3					104.2	6.0	80.0	4.9			67.0	4.6	150.7	9.7	98.6	11.3	75.3	4.5	175	6.7																													6/23/2003	MK Sullivan											7480533.05
Locomotor activity, 1 -5 min after 2 g/kg ethanol IP conditioning trial 4 (experimental group prior ethanol exposure) [activity counts per min]	table 1 col 5	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	15	56-125 days	56	125	Male	13-34	2 g/kg IP, activity counts/min	57.6	4.1	165.8	7.2	90.4	9.8	67.6	4.9	54.4	4.0	50.4	3.7	123.7	10.5	138.5	7.8	61.0	6.0	45.1	4.9	70.1	7.3	94.5	7.9	49.0	3.5	31.7	2.7	126.0	7.3					114.3	8.7	77.3	4.3			74.3	5.8	115.8	10.1	133.4	12.3	59.3	5.7	170.8	9.1																													6/23/2003	MK Sullivan											7480533.15
Locomotor activity, 1 - 5 min after single saline i.p. injection (control group) [activity/min]	table 2 col 1	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	07	56-125 days	56	125	Male	6-16	activity/min	132.9	7.5	66.0	7.2	101.1	7.0	77.5	10.8	57	7.1	117.9	9.0	52.1	3.6	85.7	10.7	50.2	6.0	87	7.5	68.1	8.6	80.6	10.7	47.4	4.3	44.8	4.0	93.1	7.5					56.3	4.0	46.1	6.9			46.9	2.7	81.8	10.3	54.3	7.5	49	3.5	141.7	9.7																													6/23/2003	MK Sullivan											7480533.07
Locomotor activity, 1 - 5 min after saline i.p., trial 1 (control group) [activity/min]	table 2 col 2	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	08	56-125 days	56	125	Male	6-16	activity/min	75.9	5.7	48.0	4.6	74.4	4.8	58.5	6.0	35.2	2.1	81.0	6.4	50.6	2.9	67.5	4.6	37.2	3.8	60.4	6.0	37.1	2.6	52.2	4.2	44.5	3.2	37.8	2.2	75.9	3.9					57.2	2.0	45.0	3.5			35.4	2.1	62.8	4.2	58.3	9.4	41.2	3.5	135.0	6.8																													6/23/2003	MK Sullivan			Saline: Trial 1								7480533.08
Locomotor activity, 1 - 5 min after saline i.p., trial 4 (control group) [activity/min]	table 2 col 3	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	09	56-125 days	56	125	Male	6-16	activity/min	37.8	3.4	39.3	5.0	41.9	3.4	26.4	3.2	22.9	2.2	38.7	4.9	28.6	3.4	41.2	3.6	14.9	2.2	35.9	4.5	15.4	2.0	33.9	3.7	33.6	2.5	25.5	1.8	58.2	4.1					41.6	2.4	30.2	4.2			20.5	3.8	36.8	3.3	22.1	3.4	30.2	4.1	97.5	8.2																													6/23/2003	MK Sullivan			Saline: Trial 4								7480533.09
Maximal threshold  to ethanol induced ataxia [mg/ml] 		Rapid tolerance to rotarod ataxia has previously been demonstrated in mice after sequential ethanol injections. Here we tested DBA/2J and C57BL/6J mice for initial ethanol sensitivity; DBA/2J mice were more sensitive (0.40 +/- 0.17 mg/g brain) than C57BL/6J mice (1.44 +/- 0.12 mg/g). We then monitored the development of tolerance by quantifying blood ethanol concentrations at the recovery from ataxia over five sequential injections; tolerance reached a plateau in about 5 hr. DBA/2J mice became very tolerant (final ethanol threshold 3.47 +/- 0.16 mg/ml, an increase of 3.07 mg/ml, or 8.7-fold above base line); B6 became slightly tolerant (final ethanol threshold 2.62 +/- 12 mg/ml, and increase of 1.18, or 1.8-fold above base line). Therefore, by the end of the treatment regimen, the rank order of sensitivity of the two strains had reversed. We then tested 25 recombinant inbred strains from among strains representing a cross between C57BL/6J and DBA/2J inbred strains, followed by a quantitative trait locus analysis with a database of 1522 markers to identify provisional loci. This procedure identified 19 markers on 11 chromosomes for initial sensitivity, 18 markers on 9 chromosomes for tolerance (delta) and 21 markers on 11 chromosomes for tolerance (fold-increase). Of these, 17 markers were in common, which suggests that initial sensitivity and tolerance share substantial genetic codetermination. Major candidate loci will be confirmed by genotyping B6D2F2 offspring that have been tested for initial sensitivity and tolerance.	Gallaher EJ, Jones GE	Mapping the genes for haloperidol-induced catalepsy.	J Pharmacol Exp Ther	277(2)	604-612	May	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627537&dopt=Abstract	8627537	96210104	02	44-135 days	44	135	Male	5-12	mg/ml	2.62		3.47		3.75		2.94		2.75		2.21		3.13		3.63		3.24		2.63		3.27		2.65		2.66		2.88		2.86		2.81				2.93		3.28		3.12		3.26		3.17		2.67		3.21		2.91		3.52		2.57		3.49																								12/19/2002												8627537.02
Mean life span [longevity in days] 		Normal somatic cells undergo replicative senescence in vitro but the significance of this process in organismic aging remains controversial. We have shown previously that hemopoietic stem cells of common inbred strains of mice vary widely in cycling activity and that this parameter is inversely correlated with strain-dependent mean life span. To assess whether cell cycling and life span are causally related, we searched for quantitative trait loci (QTLs) that contributed to variation of these traits in BXH and BXD recombinant inbred mice. Two QTLs, mapping to exactly the same intervals on chromosomes 7 and 11, were identified that were associated with variation of both cell cycling and life span. The locus on chromosome 11 mapped to the cytokine cluster, a segment that shows synteny with human chromosome 5q, in which deletions are strongly associated with myelodysplastic syndrome. These data indicate that steady-state cell turn-over, here measured in hemopoietic progenitor cells, may have a significant effect on the mean life span of mammals.	de Haan G, Van Zant G	Genetic analysis of hemopoietic cell cycling in mice suggests its involvement in organismal life span.	FASEB J	13(6)	707-713	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10094931&dopt=Abstract	10094931	99196952	02	6-8 wks	42	56	Female	10-20	days	675		175		600		400		525		690		660		825		750		740				500		800		650		740		900						740		760		840				715		760		700		740		580		200																								6/9/2003	MK Sullivan											10094931.02
Medulla weight [mg] [mean value calculated 6/29/00]			Williams RW unpub		unpublished				2000					80	100 days	100		MF		mg											5.5		8.2		8.6										6.8						5.7				7.3																						6.3		6.3		5.9		5.7				6.4		6.4		7.2				7.0				12/19/2002												.8
Mossy fiber MF		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	01	100 days	100		MF			201035		170534		235457		183237		176552		204155		241324		183084		167761		168565		182073		208777		181884		166098		166098		195597		183097		195597		167891		169252		159822		169252		159888		195822		183649		172789		206713		159736																								6/6/2002												8024533.01
Mossy fiber CA4MF		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	02	100 days	100		MF			95604		73495		108113		79558		69461		98145		102257		82676		76052		71343		80200		85196		91529		84975		72329		78205		80195		82715		77941		79350		69893		72158		67393		86697		81027		73771		89044		70752																								6/6/2002												8024533.02
Mossy fiber SPMF		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	03	100 days	100		MF			78388		93765		101833		83695		82143		92057		105625		84840		76814		75664		84697		98555		118355		77463		72642		93293		77409		92860		90151		79737		77537		75635		74170		85185		83292		83211		98742		74437																								6/6/2002												8024533.03
Mossy fiber IIPMF		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	04	100 days	100		MF			27042		12275		25512		19984		24948		13953		33443		15568		14895		21558		17176		25025		14859		19446		21127		12645		7688		20021		15005		26597		20462		21460		18326		24939		19329		15807		18926		14546																								6/6/2002												8024533.04
Mossy fiber CA4/MF %		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	05	100 days	100		MF			47.56		40.88		45.42		43.33		39.48		48.17		42.3		45.26		45.36		42.32		44.08		40.6		40.6		46.77		43.53		42.64		48.55		42.21		42.57		42.66		41.82		42.65		42.2		43.74		44.11		42.72		42.64		44.29																								6/6/2002												8024533.05
Mossy fiber SP/MF %		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	06	100 days	100		MF			39.03		52.37		43.77		45.94		46.47		45.06		43.77		46.39		45.85		44.97		46.61		47.62		52.8		42.62		43.77		50.57		46.88		47.69		49.27		43.05		46.2		44.73		46.5		43.68		45.41		48.17		48.16		46.67																								6/6/2002												8024533.06
Mossy fiber IIP/MF %		Mice of the BALB/c strain are widely used in behavioral research in spite of the albino condition, which can obscure brain-behavior relationships. We have developed a pigmented BALB strain, congenic to BALB/c, which could be more appropriate for neurogenetic studies that aim at identifying the effects of neurological mutations on behavior. Comparison of inbred albino and pigmented congenic BALB arising from the same litters provides a valuable tool for detecting the consequences of the albino mutation on behavioral performances. Preliminary results presented here show that the albino condition does not interfere with the development and patterns of connectivity of mossy fibers in the hippocampus. On the other hand, obvious coat color-linked differences appear for locomotor activity and defecation scores in the open field, pigmented mice being unexpectedly less active and more reactive than albino, as if better vision increased their reactions to a novel, anxiogenic environment. Finally, pigmented mice do not show better performances in the radial maze, which confirms that the inability of BALB mice for spatial learning in a highly demanding version of this task cannot be attributed to their inability to process visual information.	Lassalle JM,ÊHalley H,ÊRoullet P.	Analysis of behavioral and hippocampal variation in congenic albino and pigmented BALB mice.	Behav Genet	24(2)	161-169	Mar	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8024533&dopt=Abstract	8024533	94296355	07	100 days	100		MF			13.41		6.76		10.81		10.73		14.05		6.77		13.93		8.34		8.79		12.71		9.31		11.78		6.6		10.61		12.7		6.78		4.57		10.1		8.16		14.29		11.97		12.62		11.31		12.58		10.48		9.11		9		9.04																								6/6/2002												8024533.07
Lavageable bronchoalveolar polymorphonuclear leukocytes (PMNs) 6h after acute (3h) exposure to 2ppm ozone, number of PMNs [BAL (x10^3)]		We demonstrated previously that inbred strains of mice are differentially susceptible to acute (3 h) and subacute (48 h) exposures to 2 parts per million (ppm) ozone (O3) and 0.30 ppm O3, respectively. Genetic studies with O3-resistant C3H/HeJ and O3-susceptible C57BL/6J strains have indicated that susceptibility to each of these O3 exposures is under Mendelian (single gene) control. In the present study, we hypothesized that the same gene controls susceptibility to the airway inflammatory responses to 2 ppm and 0.30 ppm O3 exposures. To test this hypothesis, airway inflammation was induced in 10 BXH and 16 BXD recombinant inbred (RI) strains of mice by acute as well as subacute O3 exposures. Airway inflammation was assessed by counting the number of polymorphonuclear leukocytes (PMNs) in bronchoalveolar lavage (BAL) returns obtained immediately after 48-h subacute exposure to 0.30 ppm O3, or 6 h after 3 h acute exposure to 2 ppm O3. Each RI strain was classified as susceptible or resistant to each exposure, based on a comparison of mean numbers of PMNs with those of the respective progenitor strains. For each RI set, a phenotypic strain distribution pattern (SDP) was thus derived for each exposure regimen, and the SDPs were then compared for concordance. Among the BXH RI strains, 4 of 10 responded discordantly to the two exposures: 3 were susceptible to acute exposure and resistant to subacute exposure, whereas 1 was conversely susceptible. Among the BXD RI strains, 4 of 16 were discordant: 1 was susceptible to acute exposure, and resistant to subacute exposure, whereas 3 were conversely susceptible.(ABSTRACT TRUNCATED AT 250 WORDS)	Kleeberger SR, Levitt RC, Zhang LY.	Susceptibility to ozone-induced inflammation. II. Separate loci control responses to acute and subacute exposures	Am J Physiol	264(1Pt 1)	L21-L26	Jan	1993		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8430813&dopt=Abstract	8430813		01	6-8 wks	42	56	MF	4-38	number of PMNs in BAL (x103)	10	1.4	2	1.3	2	1.3	4	1.8					2	1.4	1	1.3	13	1.9	2	1.4							1	1.4							15	5.1					3	1.6	2	1.6	23	6.5	1	1.5	1	1.3	2	1.2	1	1.3	1	1.6																							6/25/2003	MK Sullivan											8430813.01
Lavageable bronchoalveolar polymorphonuclear leukocytes (PMNs) 6h after subacute (48h) exposure to 0.30 ppm ozone, number of PMNs [BAL (x10^3)]		We demonstrated previously that inbred strains of mice are differentially susceptible to acute (3 h) and subacute (48 h) exposures to 2 parts per million (ppm) ozone (O3) and 0.30 ppm O3, respectively. Genetic studies with O3-resistant C3H/HeJ and O3-susceptible C57BL/6J strains have indicated that susceptibility to each of these O3 exposures is under Mendelian (single gene) control. In the present study, we hypothesized that the same gene controls susceptibility to the airway inflammatory responses to 2 ppm and 0.30 ppm O3 exposures. To test this hypothesis, airway inflammation was induced in 10 BXH and 16 BXD recombinant inbred (RI) strains of mice by acute as well as subacute O3 exposures. Airway inflammation was assessed by counting the number of polymorphonuclear leukocytes (PMNs) in bronchoalveolar lavage (BAL) returns obtained immediately after 48-h subacute exposure to 0.30 ppm O3, or 6 h after 3 h acute exposure to 2 ppm O3. Each RI strain was classified as susceptible or resistant to each exposure, based on a comparison of mean numbers of PMNs with those of the respective progenitor strains. For each RI set, a phenotypic strain distribution pattern (SDP) was thus derived for each exposure regimen, and the SDPs were then compared for concordance. Among the BXH RI strains, 4 of 10 responded discordantly to the two exposures: 3 were susceptible to acute exposure and resistant to subacute exposure, whereas 1 was conversely susceptible. Among the BXD RI strains, 4 of 16 were discordant: 1 was susceptible to acute exposure, and resistant to subacute exposure, whereas 3 were conversely susceptible.(ABSTRACT TRUNCATED AT 250 WORDS)	Kleeberger SR, Levitt RC, Zhang LY.	Susceptibility to ozone-induced inflammation. II. Separate loci control responses to acute and subacute exposures	Am J Physiol	264(1Pt 1)	L21-L26	Jan	1993		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8430813&dopt=Abstract	8430813		02	6-8 wks	42	56	MF	2-16	number of PMNs in BAL (x103)	10	2.1	2	1.3	14	3.5	16	4.5					14	4.9	1	1.3	23	6.9	1	1.3							4	1.3							2	1.3					2	1.5	2	1.3	14	2.0	1	1.4	2	1.4	2	1.4	1	1.3	1	1.3																							6/25/2003	MK Sullivan											8430813.02
T cell receptor expression,  V-gamma-1 positive, V-gamma-4 positive, % of total gamma-delta intestinal intraepithelial lymphocytes [%]		Most of the gd T cells in the intestinal epithelium of normal mice use the Vg1 or the Vg7 gene segments. However, the relative proportions of  gd intraepithelial lymphocytes expressing either the Vg1 or the Vg7 chain vary among different strains of mice whereas they are quite constant between different individuals of the same strain, suggesting that genetic factors, rather than environmental factors, are responsible for the observed differences. To analyze the genetic factors influencing the representation of different gd T cell subsets in the intestinal epithelium, we used available anti-T cell antigen receptor (TCR) V region-specific mAbs against Vg1, Vg4, Vg7, and Vd4 to examine the TCR repertoire of intraepithelial gd lymphocytes in a set of (C57BL/6Ê´ÊDBA/2) recombinant inbred strains. Our results show that the representation of different Vg and Vd gene products among gd   intestinal intraepithelial lymphocytes is under a complex genetic control with a marked influence by genes closely linked to the TCRg, TCRd, and major histocompatibility complex loci. 	Pereira P, Lafaille JJ, Gerber D, and Tonegawa S	The T cell receptor repertoire of intestinal intraepithelial gammadelta T lymphocytes is influenced by genes linked to the major histocompatibility 	Proc Natl Acad Sci USA	94(11)	5761-5766	May	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9159147&dopt=Abstract	9159147		01	2-6 months	60 	180	MF	2	% 					14.75 		1.5 		3.25		4.75 		4.25		6.25 		2.25		10.75 		8.75		7.5		2.25 		2.75		8.75		1.5 				2.75 		3.75 		10.75		3.25		19.25		1.5		2.25		8.75 		9.0 		4.25 		4.25																								12/19/2002		Nathan Copeland										9159147.01
T cell receptor expression,  V-gamma-7 positive and V-gamma-4] positive % of total gamma-delta intestinal intraepithelial lymphocytes [%]		Most of the gd T cells in the intestinal epithelium of normal mice use the Vg1 or the Vg7 gene segments. However, the relative proportions of  gd intraepithelial lymphocytes expressing either the Vg1 or the Vg7 chain vary among different strains of mice whereas they are quite constant between different individuals of the same strain, suggesting that genetic factors, rather than environmental factors, are responsible for the observed differences. To analyze the genetic factors influencing the representation of different gd T cell subsets in the intestinal epithelium, we used available anti-T cell antigen receptor (TCR) V region-specific mAbs against Vg1, Vg4, Vg7, and Vd4 to examine the TCR repertoire of intraepithelial gd lymphocytes in a set of (C57BL/6Ê´ÊDBA/2) recombinant inbred strains. Our results show that the representation of different Vg and Vd gene products among gd   intestinal intraepithelial lymphocytes is under a complex genetic control with a marked influence by genes closely linked to the TCRg, TCRd, and major histocompatibility complex loci. 	Pereira P, Lafaille JJ, Gerber D, and Tonegawa S	The T cell receptor repertoire of intestinal intraepithelial gammadelta T lymphocytes is influenced by genes linked to the major histocompatibility 	Proc Natl Acad Sci USA	94(11)	5761-5766	May	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9159147&dopt=Abstract	9159147		02	2-6 months	60 	180	MF	2	% 					26.5 		6.0 		13.0		5.0 		7.5		9.0 		9.0 		8.5		13.0 		3.5 		8.5 		9.5 		7.5 		9.0 				12.0 		22.5		20.5		19.5 		15.0 		16.5 		30.5		6.0 		21.5 		7.5 		8.5 																								12/19/2002		Nathan Copeland										9159147.02
T cell receptor expression,  V-gamma-7 positive, Vgamma-4 negative, % of total gamma-delta intestinal intraepithelial lymphocytes [%]		Most of the gd T cells in the intestinal epithelium of normal mice use the Vg1 or the Vg7 gene segments. However, the relative proportions of  gd intraepithelial lymphocytes expressing either the Vg1 or the Vg7 chain vary among different strains of mice whereas they are quite constant between different individuals of the same strain, suggesting that genetic factors, rather than environmental factors, are responsible for the observed differences. To analyze the genetic factors influencing the representation of different gd T cell subsets in the intestinal epithelium, we used available anti-T cell antigen receptor (TCR) V region-specific mAbs against Vg1, Vg4, Vg7, and Vd4 to examine the TCR repertoire of intraepithelial gd lymphocytes in a set of (C57BL/6Ê´ÊDBA/2) recombinant inbred strains. Our results show that the representation of different Vg and Vd gene products among gd   intestinal intraepithelial lymphocytes is under a complex genetic control with a marked influence by genes closely linked to the TCRg, TCRd, and major histocompatibility complex loci. 	Pereira P, Lafaille JJ, Gerber D, and Tonegawa S	The T cell receptor repertoire of intestinal intraepithelial gammadelta T lymphocytes is influenced by genes linked to the major histocompatibility 	Proc Natl Acad Sci USA	94(11)	5761-5766	May	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9159147&dopt=Abstract	9159147		03	2-6 months	60 	180	MF	2	% 					24.0		49.5		21.0		17.5 		57.0 		27.5 		36.5 		27.5 		43.0		38.0 		52.5		34.0 		26.0		58.5				22.0 		26.0 		41.0 		34.0		24.0 		29.5 		31.5		43.0 		27.5 		31.5 		22.5 																								12/19/2002		Nathan Copeland										9159147.03
T cell receptor expression,  V-gamma-1 positive, V-gamma-4 negative, % of total gamma-delta intestinal intraepithelial lymphocytes [%]		Most of the gd T cells in the intestinal epithelium of normal mice use the Vg1 or the Vg7 gene segments. However, the relative proportions of  gd intraepithelial lymphocytes expressing either the Vg1 or the Vg7 chain vary among different strains of mice whereas they are quite constant between different individuals of the same strain, suggesting that genetic factors, rather than environmental factors, are responsible for the observed differences. To analyze the genetic factors influencing the representation of different gd T cell subsets in the intestinal epithelium, we used available anti-T cell antigen receptor (TCR) V region-specific mAbs against Vg1, Vg4, Vg7, and Vd4 to examine the TCR repertoire of intraepithelial gd lymphocytes in a set of (C57BL/6Ê´ÊDBA/2) recombinant inbred strains. Our results show that the representation of different Vg and Vd gene products among gd   intestinal intraepithelial lymphocytes is under a complex genetic control with a marked influence by genes closely linked to the TCRg, TCRd, and major histocompatibility complex loci. 	Pereira P, Lafaille JJ, Gerber D, and Tonegawa S	The T cell receptor repertoire of intestinal intraepithelial gammadelta T lymphocytes is influenced by genes linked to the major histocompatibility 	Proc Natl Acad Sci USA	94(11)	5761-5766	May	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9159147&dopt=Abstract	9159147		04	2-6 months	60 	180	MF	2	% 					36.5 		34.5		55.5		67.5		39.0		55.5 		49.0		49.0		31.0		41.5 		33.5 		61.5 		51.0		33.5				57.5 		41.5 		35.5		34.0		35.5		44.0 		40.0 		32.0 		36.5 		51.0 		54.5 																								12/19/2002		Nathan Copeland										9159147.04
T cell receptor expression,  V-gamma-7 positive, gamma-4 negative cells, % of total gamma-delta intestinal intraepithelial lymphocytes [%]		Most of the gd T cells in the intestinal epithelium of normal mice use the Vg1 or the Vg7 gene segments. However, the relative proportions of  gd intraepithelial lymphocytes expressing either the Vg1 or the Vg7 chain vary among different strains of mice whereas they are quite constant between different individuals of the same strain, suggesting that genetic factors, rather than environmental factors, are responsible for the observed differences. To analyze the genetic factors influencing the representation of different gd T cell subsets in the intestinal epithelium, we used available anti-T cell antigen receptor (TCR) V region-specific mAbs against Vg1, Vg4, Vg7, and Vd4 to examine the TCR repertoire of intraepithelial gd lymphocytes in a set of (C57BL/6Ê´ÊDBA/2) recombinant inbred strains. Our results show that the representation of different Vg and Vd gene products among gd   intestinal intraepithelial lymphocytes is under a complex genetic control with a marked influence by genes closely linked to the TCRg, TCRd, and major histocompatibility complex loci. 	Pereira P, Lafaille JJ, Gerber D, and Tonegawa S	The T cell receptor repertoire of intestinal intraepithelial gammadelta T lymphocytes is influenced by genes linked to the major histocompatibility 	Proc Natl Acad Sci USA	94(11)	5761-5766	May	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9159147&dopt=Abstract	9159147		05	2-6 months	60 	180	MF	2	%					27.0		49.5		21.5		17.5				27.0		36.5		27.0		43.0		38.0				34.5		25.5						23.0		26.0		41.0		34.0		24.0		30.0		30.5		45.5		23.5		31.5		22.5																								12/19/2002		Nathan Copeland										9159147.05
Olfactory bulb weight, mg [raw average from strainDB 6/28/00]		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		01	80 days	80		MF	349 males and 321 females	mg					20.9		23.1		22.3		21.2		20.2		22.0		17.7		20.3		18.0		18.7		18.8		21.5		21.1		18.7		18.2		18.9		21.0				16.9		17.6		17.9		19.1		19.1		17.8		20.4		21.7		20.3		23.0		24.0		17.5		23.0		22.4		19.5		22.0				20.9				6/12/2003	MK Sullivan											11529276.01
Olfactory Bulb Weight, adjusted [mg]		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L.	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		02	80 days	80		MF	349 males and 321 females	mg	21.9	0.4	21.6	0.3	20.7	0.2	21.1	0.7	18.3	0.5	22.0	0.4	19.3	0.2	20.0	0.4	18.7	0.4	20.0	0.5	19.4	0.2	19.9	0.5	18.0	0.5	19.7	0.4	21.0	0.4	18.6	0.6	20.9	0.5	17.3	0.5	19.8	0.7	18.7	0.5	18.6	0.7	18.3	0.5	20.3	0.3	19.7	0.4	20.1	0.6	20.7	0.6	21.4	0.6	20.1	0.3	20.3	0.4	23.2	0.4	23.6	1.0	18.1	0.5	21.2	2.0	22.5	0.7	20.4	0.3	20.3	0.7			19.3	0.1			6/12/2003	MK Sullivan											11529276.02
Olfactory Bulb Weight CV%		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L.	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		03	80 days	80		MF	349 males and 321 females	%	4.8		4.4		1.4		3.5		4.2		3.0		3.2		3.5		2.3		2.1		2.9		3.5		2.3		4.7		3.3		4.2		3.4		4.7		3.3		4.2		1.1		3.0		2.5		3.4		2.7		3.6		3.7		4.6		1.8		2.6		1.3		1.3		1.7		3.4		0.4		2.4				2.0				6/12/2003	MK Sullivan											11529276.03
Olfactory Bulb Weight, unadjusted [mg]		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L.	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		04	80 days	80		MF	349 males and 321 females	mg	22.7		19.8		21.6		21.2		21.2		20.3		22.6		21.7		18.6		20.4		18.5		20.9		19.0		21.7		22.2		18.6		18.8		17.9		20.8		18.1		17.3		17.4		17.7		19.2		19.1		18.6		21.0		19.8		21.0		23.8		24.4		18.2		19.9		23.1		20.4		21.7				21.4				6/12/2003	MK Sullivan											11529276.04
Brain Weight [mg]		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L.	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		05	80 days	80		MF	349 males and 321 females	mg	495		415		456		440		502		391		498		469		420		447		402		439		449		467		445		432		382		442		444		420		394		410		375		413		403		382		415		432		445		439		449		427		428		437		423		464				469				6/12/2003	MK Sullivan											11529276.05
Body Weight [g]		Olfaction is influenced by a complex mix of environmental and genetic factors that modulate the production, migration, and maturation of cells in the olfactory bulbs. In this study we analyzed effects of sex, age, body weight, and brain weight on olfactory bulb size in sexually mature mice. We then used regression corrected values (residuals) to map quantitative trait loci (QTLs) that selectively modulate bulb weight. This biometric analysis has relied on an F2 intercross between C57BL/6J (B6) and DBA/2J (D2) inbred strains and a large sample of 35 BXD recombinant inbred (RI) strains. Bilateral bulb weight in adult mice ranges from 10 to 30 mg. Half of this remarkable variation can be predicted from differences in brain weight, sex, body weight, and age. A 100-mg difference in brain weight is associated with a 4.4-mg difference in bulb weight. Bulbs gain in weight by 0.2 mg/week--a 1% increase that continues until at least 300 days of age. Males tend to have slightly larger bulbs than females. By combining data from both related crosses (F2 and RI) we identified four QTLs with selective effects on bulb size (genomewide p < .05). Bulb4a is located on chromosome 4 (Chr 4) and Bulb6a is located on Chr 6. Alleles inherited from B6 at both of these loci increase bulb weight by 0.5-1.0 mg. Bulb11a is located on proximal Chr 11 and Bulb17a is located on the proximal part of Chr 17. In contrast to the first two QTLs, B6 alleles at these two loci decrease bulb weight by 0.5-1.0 mg. Collectively, the four loci account for 20% of the phenotypic variance in bulb weight.	Williams RW, Airey DC, Kulkarni A, Zhou G, Lu L.	Genetic dissection of the olfactory bulbs of mice: QTLs on four chromosomes modulate bulb size.	Behav Genet	31(1)	61-77	Jan	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11529276&dopt=Abstract	11529276		06	80 days	80		MF	349 males and 321 females	g	24.7		19.3		18.8		28.9		22.2		19.9		22.9		23.6		18.8		21.2		19.5		21.7		24.3		23.9		21.3		21.2		19.0		21.8		20.3		20.0		20.7		19.2		20.2		23.1		22.3		18.2		20.8		26.0		17.7		21.1		25.8		17.2		22.5		19.4		20.2		20.2				21.0				6/12/2003	MK Sullivan											11529276.06
Open-field activity following saline injection [number of crossings during 3 min]		Recombinant inbred (RI) strains are valuable not only for detecting major gene segregation and linkage but also for identifying associations between behavior and quantitative trait loci (QTL) that account for relatively small amounts of variation in behaviors for which strain distribution patterns are not bimodal. When applied to published data on genetic markers and on behavior for BXD RI strains, the RI QTL association approach suggests the presence of QTLs on chromosomes 6 and 12 for open-field activity and on chromosomes 1, 2, and 17 for high-pressure seizure susceptibility. Because the RI QTL approach does not require that the progenitor inbred strains of a particular RI series differ, researchers could focus on the BXD RI series, for which the greatest number of genetic markers are available. Focusing on BXD would capitalize on the cumulative nature of RI research which permits analyses of QTL sources of genetic correlations across studies.	Plomin R, McClearn GE,ÊGora-Maslak G,Ê Neiderhiser JM.	Use of recombinant inbred strains to detect quantitative trait loci associated with behavior.	Behav Genet	277(2)	99-116	Mar	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2049054&dopt=Abstract	2049054	91264768	02	100 days	100				number of crossings during 3 min	160		140		180		180		190		160		120				80		140		120		160		100		160		140		160				180				160		120				140		80		180		100																												7/14/2003	MK Sullivan											2049054.02
Plasma corticosterone levels 6 hr post 4 g/kg Ethanol [µg/dl]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	05	65-115 days	65	115	Male	5-15	µg/dl	7	1.03	10.5	1.43	7.5	2.65			10	1.34	10	1.61	6	1.97	12	2.92	3.5	.94	10.5	1.38			7.5	1.20	8	1.35	7.5	1.49	7.5	.67	5	.83			6	1.25					10.5	2.36	3	1.03	4.5	1.68	7.5	1.22	10	.75	7.5	3.07	4	.83	4	1.60																							12/26/2002												8748968.05
Plasma corticosterone levels 6 hr post saline [µg/dl]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav  Neurosci	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	06	65-115 days	65	115	Male	3-9	µg/dl	1	1.22	7.5	0.86	1	1.58			6	.71	2.5	.71	2	.39	3.5	0.00	3	1.07	2	1.06			5.5	1.05	4.5	0.83	3.5	1.30	6	.977	2	0.80			2.5	1.16					3.5	1.79	2.5	1.00	4	1.00	3	1.04	1.5	1.14	5	0.91	4	1.07	4.5	0.98																							12/26/2002												8748968.06
Plasma corticosterone levels 7 hr post 4 g/kg  Ethanol [µg/dl]		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	07	65-115 days	65	115	Male	5-15	µg/dl	7	1.37	12	1.90	4	1.45	10	2.07	12	3.68	12.5	2.35	5	1.04	13	2.87	10	2.10	9.5	2.40	6	0.63	6	1.08	9	2.06	7	1.04	5.5	0.77	4	1.42			8	0.87	9.5	2.99			15	3.42			24.5	4.72	8	1.58	15.5	1.69	16	2.00	8.5	3.16	13	2.10																							12/26/2002												8748968.07
Handling-induced convulsion scores 7 hr post 4 g/kg Ethanol		The genetic control over the corticosterone response to ethanol (EtOH) and its possible relationship to other EtOH-related traits was examined using BXD recombinant inbred (RI) strains derived from an F2 cross of C57BL/6J (B6) and DBA/2J (D2) progenitor strains. Quantitative trait locus (QTL) analysis of corticosterone levels 1 hr following EtOH suggested the influence of a single major gene on this trait. Two loci were predicted to account for 47% of the genetic variance in plasma corticosterone levels 6 hr following EtOH, whereas 3 loci were predicted to account for 78% of the genetic variance in corticosterone levels 7 hr following EtOH. Markers associated with corticosterone levels 7 hr following EtOH and corrected corticosterone levels 6 hr post-EtOH overlapped with ones found to influence acute and chronic EtOH withdrawal severity, suggesting some degree of common genetic determination between these traits. Overall these results indicate that gene action significantly influences stress responsiveness and suggest possible chromosomal locations of these genes.	Roberts AJ, Phillips TJ, Belknap JK, Finn DA, Keith LD.  	Genetic analysis of the corticosterone response to ethanol in BXD recombinant inbred mice	Behav Neurosci	109(6)	1199-1208	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748968&dopt=Abstract	8748968	96350725	08	65-115 days	65	115	Male	5-15		0.2	0.19	3	0.19	0.8	0.29	2.4	0.75	0.9	0.15	0	0	0.9	0.23	2	0.25	0.7	0.15	0.4	0.20	1.8	0.37	1.4	0.28	0.9	0.08	0.4	0.22	0.3	0.14	0	0			0.9	0.27	0.8	0.15			0	0			1.2	0.18	0.8	0.16	0.1	0.07	2.3	0.21	0	0	1.8	0.41																							12/26/2002												8748968.08
Preconditioned stimulus [% freezing]		Fear conditioning shows associations formed between contextual or auditory stimuli with an unconditioned stimulus. Inbred mouse strains differ in their ability to demonstrate fear conditioning, suggesting at least a partial genetic influence. The present study identified the possible chromosomal loci regulating fear conditioning in BXD recombinant inbred strains using quantitative trait loci (QTL) analysis. Estimates of heritability for all 3 measures of conditioning were about .28. Correlational analyses between genetic markers and strain means identified multiple putative QTLs. The strongest associations were on Chromosomes 1 and 17 for freezing to the context, Chromosome 12 for freezing to an altered context, and Chromosome 1 for freezing to the auditory stimulus. Overlapping QTLs may indicate some common genes that underlie aspects of this learning task.	Owen EH, Christensen SC, Paylor R, Wehner JM	Identification of quantitative trait loci involved in contextual and auditory-cued fear conditioning in BXD recombinant inbred strains.	Behav Neurosci 	111(2)	292-300	Apr	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9106670&dopt=Abstract	9106670	97260550	03	60-134 days 	60	134	MF	9-20	% freezing	32	0.423	10	0.200	5	1.69	11	2.31			5	1.38	30	12.00	15	3.23	22	5.00	7	2.00	20	4.46	6	2.00			17	2.58			6	2.08			27	6.62	35	4.62	35	6.77	15	3.46	10	3.34	32	3.62	32	4.31	0	0.00	5	1.69			40	5.31																							6/12/2003	MK Sullivan											9106670.03
Floor preference test - average time on grid floor (control group) [s/min]	table 2 col 4	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	14	56-125 days	56	125	Male	6-16	s/min	29.6	2.4	33.4	2.7	31.3	3.1	35.2	3.5	26.9	2.6	33.7	3.1	28.6	2.3	32.4	2.0	30.7	2.7	26.5	3.1	24.7	1.8	29.7	1.8	25.6	1.6	27.3	3.6	31.3	1.3					28.8	1.5	23.2	3.4			38.0	3.2	31.5	2.3	31.6	4.0	32.1	3.2	31.5	1.4																													6/23/2003	MK Sullivan											7480533.14
Floor preference test, average time on grid textured floor (control group) [s/min]	table 2 col 5	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	16	56-125 days	56	125	Male	6-16	s/min	41.5	3.8	40.2	1.8	29.4	2.4	30.1	3.5	29.3	1.6	31.4	2.9	33.4	1.3	43.8	3.2	29.0	1.5	40.0	4.2	30.6	2.2	40.7	2.9	29.5	1.7	24.1	1.6	48.0	2.7					37.9	1.8	26.6	2.3			20.9	2.4	34.8	2.4	38.3	4.5	31.7	2.1	66.8	5.7																													6/23/2003	MK Sullivan											7480533.16
Floor preference test - preference for grid textured floor in Conditioned Place Preference Apparatus (experimental group)[activity/min]	table 3 col 3	Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	06	56-125 days	56	125	Male	7-17	activity/min	38.5	2.5	42.8	2.4	31.0	1.9	37.8	2.5	27.9	0.9	31.4	1.4	33.5	1.8	47.3	1.9	25.8	1.7	37.1	2.9	26.8	1.9	40.2	2.5	30.1	1.5	21.2	1.4	52.2	2.3					39.9	1.7	26	1.4			22.9	1.3	36.2	2.1	42.3	2.8	32.7	2.2	88.7	4.1																													6/23/2003	MK Sullivan											7480533.06
Granulocyte Colony Stimulating Factor induced   Progenitor cell mobilization from bone marrow to blood [PB-CFC/µl]		Granulocyte colony-stimulating factor (G-CSF) can effectively mobilize hematopoietic stem and progenitor cells from bone marrow into blood, thereby allowing peripheral blood stem cells (PBSCs) to be used for transplantation. The efficiency of PBSC mobilization response to G-CSF is a multigene trait. DBA/2 (high-responder) and C57BL/6 (low-responder) mice were used for a genetic analysis of G-CSF-induced progenitor release. Significant linkages were found on chromosome 2Êby analyzing segregation distortion among the high responders of 500Êbackcross mice and on chromosome 11Êby using the quantitative trait locus analysis of 26Êstrains of BXD recombinant inbred mice. 	Hasegawa M,  Baldwin TM, Metcalf D, Foote SJ	Progenitor cell mobilization by granulocyte colony-stimulating factor controlled by loci on chromosomes 2 and 11.	Blood 	95(5)	1872-1874	Mar	2000		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10688851&dopt=Abstract	10688851		01	7-11 wks	49	77	MF	2-3	PB-CFC/µl					0.6		0.5		0.5		1.0		0.6		6.8		0.7		0.6		0.9		3.6		2.1		4.0		2.0		1.4		3.1		1.2		1.0		6.7		5.2		1.4		2.5		1.6		2.8		1.0		2.2																										7/7/2003	MK Sullivan	Nathan Copeland										10688851.01
Retinal area [mm2]		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	05	106 days	106		MF	8-35	mm^2	18.5		20.1		19.8		20.2		19.1		19.8		18.6		19.3		20.2		18.9		19.3		18.7		19.3		19		18.1		19.7		18.8		16.2		19.5		18.2		17		17.6		18.9		17.8		19.3		18.4		19.2		19.3																								6/12/2003	MK Sullivan											10102277.05
Retinal ganglion cell number [cells x1000]		Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells.	Williams RW, Strom RC., Goldowitz D	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	J Neurosci	18(1)	138-46	Jan	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9412494&dopt=Abstract	9412494	98075112	02	100 days	100		MF	5-11	cells x1000	55.4	0.8	63.4	1.2	60.3	1.1	65.9	1.8	75.5	1.3	62.7	0.9	62.8	2.1	65.6	1.7	61	1.1	56.8	2.1	54.7	1.7	64	1.6	63.8	1.1	64	1.3	55.1	0.9	67.1	1.3	59.9	1.9	60	1.5	64.5	1.1	53	1.0	62.4	1.0	53.8	1.5	50.8	1.1	52.4	1.9	63.6	1.4	66	1.3	66.6	1.2	75.8	2.2																							6/18/2003	MK Sullivan											9412494.02
Retinal ganglion cell number (x1000)		PURPOSE: Vision is critically dependent on genetic factors that influence the rate and duration of eye growth. The genetic basis of variation in eye size in mice was explored, and genes that modulate eye weight, lens weight, and retinal area were mapped. METHODS: Eyes of approximately 700 mice were weighed. Data were corrected by regression analysis to eliminate effects of sex, age, and body weight. Interval mapping was used to locate quantitative trait loci (QTLs) using recombinant inbred strains and F2 intercrosses between strains C57BL/6J and DBA/2J. RESULTS: Major QTLs were discovered near the centromere of chromosome 5 (Eye1: genomewide P < 0.005) and on proximal chromosome 17 near the mast cell protease 6 gene (Eye2, P < 0.05). Both QTLs have significant effects on eye size, lens weight, and retinal area. The DBA/2J alleles at Eye1 and Eye2 are partially dominant and increase eye weight by as much as 1.0 mg. Analysis of 183 F2 progeny confirmed and refined the chromosomal assignments of both Eye1 and Eye2. CONCLUSIONS: Eye1 and Eye2 are the first loci known to control normal variation in eye size in any mammal. The hepatic growth factor gene (Hgf), a potent mitogen expressed in the retina, pigment epithelium, and choroid, is a strong candidate for Eye1. The human homolog of Eye2 should map to chromosome 6p, 16q13.3, or 19q13, whereas that of Eye1 should map to 7q.	Zhou G, Williams RW	Eye1 and Eye2: gene loci that modulate eye size, lens weight, and retinal area in the mouse.	Invest Ophthalmol Vis Sci	40(5)	817-825	Apr	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10102277&dopt=Abstract	10102277	99200400	06	106 days	106		MF	8-35	x1000	55.4		63.4		60.3		65.9		75.5		62.7		62.8		65.6		61		56.8		54.7		64		63.8		64		55.1		67.1		59.9		60		64.5		53		62.4		53.8		50.8		52.4		63.6		66		66.6		75.8																								6/12/2003	MK Sullivan											10102277.06
Saccharin intakes post-saline, pre-exposed to saccharin, group 0 g/kg and trial 1 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	01	56-125 days	56	125	Male	5-12	ml	3.44	0.15	2.47	0.19	3.14	0.21	3.35	0.25	3.2	0.14	2.87	0.08	2.36	0.12	3.33	0.22	3.26	0.17	2.69	0.23	3.1	0.11	3.85	0.14	3.84	0.22	3.32 	0.20	3.79	0.29					3	0.43					2.71	0.21 	3.09	0.13	2.75	0.17	2.56	0.20	3.57	0.26					3.55	0.26																							12/26/2002			SACSsaccharin									9756038.01
Saccharin intakes post-saline, pre-exposed to saccharin, group 0 g/kg and trials 2-4 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	02	56-125 days	56	125	Male	5-12	ml	3.15	0.15	2.77	0.15	2.84	0.23	3.74	0.36	3.25	0.21	2.88	0.09	2.41	0.13	3.46	0.21	3.09	0.08	2.54	0.18	2.87	0.11	3.75	0.08	3.93	0.12	3.02	0.13	3.66	0.23					3.08	0.48					2.6	0.16	2.47	0.12	2.63	0.17	2.73	0.15	3.2	0.19					3.7	0.25																							12/26/2002			SACSsaccharin									9756038.02
Ethanol induced conditioned taste aversion to saccharin, group 2 g/kg and trial 1 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	03	56-125 days	56	125	Male	4-20	ml	3.22	0.22	3.01	0.13	3.13	0.19	3.75	0.31	3.4	0.21	2.79	0.10	2.71	0.20	3.03	0.20	3.45	0.21	2.88	0.23	3.63	0.24	3.85	0.26	3.71	0.18	2.72	0.15	3.67	0.20					3.03	0.26					2.69	0.14	3.03	0.15	2.69	0.14	2.81	0.19	3.2	0.19					3.26	0.21																							12/26/2002			SACSsaccharin									9756038.03
Ethanol induced conditioned taste aversion to saccharin, group 2 g/kg and trial 2-4 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	04	56-125 days	56	125	Male	4-20	ml	2.99	0.12	2.83	0.11	2.87	0.19	3.44	0.46	2.24	0.27	2.49	0.11	2.75	0.20	2.69	0.28	2.73	0.13	2.55	0.13	3.34	0.25	3.16	0.19	3.47	0.14	2.82	0.14	3.24	0.24					2.8	0.19					2.32	0.17	2.14	0.12	2.62	0.12	2.55	0.22	3.08	0.11					3.04	0.12																							12/26/2002			SACSsaccharin									9756038.04
Ethanol induced conditioned taste aversion to saccharin, group 4 g/kg and trial 1 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	05	56-125 days	56	125	Male	5-17	ml	3.49	0.13	2.79	0.15	2.87	0.21	3.84	0.39	3.8	0.15	2.94	0.16	2.44	0.17	3.36	0.25	3.26	0.04	2.79	0.18	3.68	0.27	4.41	0.13	3.56	0.21	3.02	0.15	3.47	0.23					3.22	0.29					3.03	0.25	2.99	0.12	2.62	0.12	2.66	0.19	3.39	0.15					3.21	0.13																							12/26/2002			SACSsaccharin									9756038.05
Ethanol induced conditioned taste aversion to saccharin, group 4 g/kg and trials 2-4 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	06	56-125 day s	56	125	Male	5-17	ml	2.64	0.06	1.66	0.12	2.39	0.17	2.8	0.28	1.59	0.16	2.28	0.14	2.28	0.10	2.22	0.36	2.37	0.10	2.18	0.15	2.28	0.23	2.78	0.21	2.39	0.16	2.78	0.14	2.88	0.23					2.37	0.21					1.9	0.20	1.8	0.07	2.26	0.17	2.18	0.19	2.14	0.21					2.00	0.18																							12/26/2002			SACSsaccharin									9756038.06
Saccharin intake post EtOH no saccharin pre-exposure group UP and trial 1 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	07	56-125 days	56	125	Male	4-12	ml	2.93	0.09	3.2	0.17	2.8	0.20	3.3	0.15	3.41	0.14	2.77	0.11	2.74	0.23	3.16	0.18	2.83	0.16	3.2	0.23	3.1	0.23	3.47	0.30	3.79	0.16	3.16	0.20	2.94	0.20					2.61	0.20					2.58	0.18	3.12	0.18	2.74	0.22	2.41	0.17	3.33	0.18					3.49	0.20																							12/26/2002			SACSsaccharin									9756038.07
Saccharin intake post EtOH no saccharin pre-exposure group UP and trials 2-4 [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	08	56-125 days	56	125	Male	4-12	ml	2.92	0.07	3.41	0.14	2.62	0.14	2.99	0.51	2.89	0.19	2.81	0.08	2.33	0.17	3.12	0.21	2.78	0.20	2.87	0.20	2.64	0..21	3.08	0.16	3.66	0.18	2.84	0.15	2.7	0.31					2.68	0.22					2.57	0.19	2.39	0.13	2.82	0.17	2.4	0.28	3.31	0.13					2.96	0.21																							12/26/2002			SACSsaccharin									9756038.08
Saccharin (0.019 % w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	09	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.81	0.06	0.56	0.17	0.41	0.06	0.43	0.13	0.88	0.06	0.84	0.11	0.58	0.08	0.6	0.10	0.91	0.04	0.59	0.09	0.65	0.13	0.63	0.07	0.77	0.13	0.44	0.09	0.68	0.11					0.54	0.16					0.64	0.08	0.62	0.09	0.73	0.12	0.59	0.13	0.61	0.14					0.58	0.11																							12/26/2002			SACSsaccharin									9756038.09
Saccharin (0.038 % w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	10	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.80	0.08	0.37	0.21	0.71	0.03	0.6	0.10	0.95	0.02	0.92	0.02	0.49	0.10	0.81	0.08	0.96	0.01	0.64	0.08	0.46	0.12	0.67	0.07	0.92	0.03	0.56	0.08	0.52	0.11					0.64	0.14					0.8	0.06	0.84	0.05	0.57	0.13	0.5	0.14	0.64	0.12					0.52	0.13																							12/26/2002			SACSsaccharin									9756038.1
Saccharin (0.076 % w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	11	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.90	0.05	0.66	0.22	0.72	0.08	0.78	0.06	0.99	0.00	0.95	0.00	0.78	0.09	0.89	0.04	0.99	0.00	0.85	0.04	0.79	0.07	0.81	0.04	0.85	0.13	0.75	0.06	0.85	0.08					0.66	0.09					0.93	0.03	0.9	0.05	0.88	0.06	0.62	0.14	0.9	0.07					0.72	0.12																							12/26/2002			SACSsaccharin									9756038.11
Saccharin (0.152 % w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	12	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.97	0.01	0.73	0.14	0.92	0.04	0.89	0.05	0.99	0.00	0.94	0.05	0.78	0.08	0.96	0.01	1	0.00	0.87	0.05	0.87	0.03	0.89	0.03	0.96	0.02	0.79	0.07	0.82	0.09					0.86	0.05					0.98	0.01	0.98	0.00	0.93	0.02	0.87	0.03	0.81	0.14					0.76	0.12																							12/26/2002			SACSsaccharin									9756038.12
Saccharin (0.304 % w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	13	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.98	0.00	0.72	0.22	0.95	0.03	0.95	0.01	0.98	0.01	0.99	0.01	0.96	0.02	0.96	0.02	0.99	0.00	0.94	0.02	0.93	0.02	0.9	0.07	0.87	0.11	0.93	0.02	0.93	0.05					0.92	0.03					0.99	0.00	0.99	0.00	0.96	0.02	0.91	0.05	0.93	0.06					0.95	0.01																							12/26/2002			SACSsaccharin									9756038.13
Saccharin (0.608% w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	14	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.99	0.00	0.85	0.05	0.98	0.01	0.98	0.01	0.99	0.00	0.98	0.00	0.93	0.05	0.89	0.10	1	0.00	0.94	0.02	0.97	0.01	0.97	0.01	0.98	0.01	0.91	0.02	0.95	0.04					0.94	0.02					0.99	0.00	0.98	0.01	0.99	0.00	0.9	0.04	0.96	0.02					0.84	0.10																							12/26/2002			SACSsaccharin									9756038.14
Saccharin (1.216% w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	15	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.98	0.01	1	0.00	0.97	0.01	0.97	0.02	0.99	0.01	0.99	0.00	0.95	0.03	0.8	0.12	0.99	0.00	0.97	0.01	0.95	0.02	0.98	0.01	0.85	0.13	0.95	0.02	0.96	0.03					1	0.00					0.99	0.00	0.98	0.00	0.88	0.07	0.91	0.04	0.97	0.02					0.97	0.02																							12/26/2002			SACSsaccharin									9756038.15
Saccharin (2.432% w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	16	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.80	0.08	0.33	0.06	0.87	0.05	0.59	0.09	0.83	0.05	0.97	0.01	0.58	0.10	0.26	0.08	0.93	0.03	0.75	0.08	0.69	0.12	0.38	0.02	0.61	0.12	0.48	0.08	0.54	0.09					0.65	0.16					0.94	0.02	0.9	0.03	0.42	0.09	0.75	0.05	0.73	0.14					0.43	0.13																							12/26/2002			SACSsaccharin									9756038.16
Saccharin (4.864% w/v) vs. tap water preference ratios [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	17	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.14	0.00	0.06	0.00	0.1	0.04	0.09	0.03	0.23	0.05	0.4	0.11	0.2	0.04	0.04	0.00	0.38	0.05	0.23	0.09	0.18	0.07	0.11	0.02	0.17	0.05	0.12	0.03	0.08	0.02					0.22	0.08					0.26	0.04	0.44	0.00	0.16	0.00	0.29	0.06	0.24	0.06					0.04	0.01																							12/26/2002			SACSsaccharin									9756038.17
Saline induced locomotor response distance traveled, 0-5 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	11	8-12wks	56	84	Male	4-18	cm	5131	284	2170	173	4018	428			1876	235	2893	263	1784	156	3817	249	1647	198	3998	847	2876	146	3481	261	1086	174	1603	225	3117	356	2888	241	2713	237	1929	99	1926	226	2511	305	2317	245	2391	199	2194	233	1449	177	4543	298	2128	184	2099	251	1559	131																							6/6/2003	MK Sullivan		SALBsaline									9880575.11
Saline induced locomotor response distance traveled, 5 - 10 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	12	8-12wks	56	84	Male	4-18	cm	3595	248	1894	136	2908	266			1767	243	2469	243	1807	158	3533	220	1333	147	2730	662	2356	149	2640	158	892	106	1752	159	3032	222	2900	204	2367	223	2200	91	1859	247	1864	244	1854	214	2316	220	1925	184	1645	140	4018	343	2143	171	2266	186	1789	149																							6/6/2003	MK Sullivan		SALBsaline									9880575.12
Saline induced locomotor response distance traveled, 10-15 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	13	8-12wks	56	84	Male	4-18	cm	2783	173	1582	138	2391	183			1442	250	2302	157	1753	162	2865	137	1166	166	2391	448	1806	145	2433	179	865	106	1612	146	2775	211	2625	185	1868	217	1852	147	1430	168	1573	217	1418	195	1752	214	1691	188	1476	173	3395	286	1850	226	2013	185	1657	127																							6/6/2003	MK Sullivan		SALBsaline									9880575.13
Saline induced locomotor response distance traveled, 15 -20 min time interval [cm] 		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	14	8-12wks	56	84	Male	4-18	cm	2580	186	1317	109	1964	123			1420	226	2272	196	1656	158	2531	175	1268	209	2084	584	2148	218	2658	205	954	80	1383	171	2642	227	2442	165	1794	187	1781	182	1347	115	1351	154	1340	233	1594	169	1797	254	1519	129	3083	280	1598	204	1775	161	1770	162																							6/6/2003	MK Sullivan		SALBsaline									9880575.14
Saline induced locomotor response distance traveled, 5-20 min time interval [cm]		A two-stage strategy was used to identify and confirm quantitative trait loci (QTLs) associated with the changes in locomotor activity induced by a 1.5 gm/kg ethanol challenge. For stage 1, putative QTLs were identified by analysis of the strain means for 25 strains of the BXD recombinant inbred (RI) series (males only). QTLs were identified on chromosomes 1, 2, 4, and 6. The activity response to chlordiazepoxide generated similar QTLs on chromosomes 2 and 6. None of the QTLs were similar to those generated from analysis of the saline response data. For stage 2, 900 male C57BL/6J (B6) x DBA/2J (D2) F2 intercross animals were phenotyped for ethanol response, and the phenotypic extremes (those animals > and <1 SD from the mean) were identified. These extremes differed by >10,000 cm/15 min in their response to ethanol. The extreme progeny were used for a genome-wide scan both to confirm the putative RI-generated QTLs and to detect new QTLs. The F2 analysis generated no new QTLs with logarithm of the likelihood for linkage (LOD) scores >3. For RI-generated QTLs, only the QTL on chromosome 2 was confirmed (LOD = 5.3). The position of the peak LOD was estimated to be 47 cM with a 20 cM 1 LOD support interval; this QTL accounted for 6% of the phenotypic variance. The 1 LOD support interval overlaps with QTLs previously identified for alcohol preference and acute ethanol withdrawal (;; ).	Demarest K,ÊMcCaughran J,ÊMahjubi E,ÊCipp L,ÊHitzemann R.	Identification of an acute ethanol response quantitative trait locus on mouse chromosome 2.	J Neurosci	19(2)	549-561	Jan	1999		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9880575&dopt=Abstract	9880575	99098941	15	8-12wks	56	84	Male	4-18	cm	8958	607	4793	383	7263	572			4629	718	7043	596	5216	477	8929	531	3767	522	7204	1694	6311	512	7731	541	2710	293	4747	477	8449	660	7966	553	6029	627	5833	419	4636	530	4787	615	4612	641	5663	603	5413	615	4640	443	10496	909	5590	601	6055	531	5215	438																							6/6/2003	MK Sullivan		SALBsaline									9880575.15
Seizure susceptibility to high atmospheric pressure at 100 atmospheres [measured at atm which seizure occurred]		Recombinant inbred (RI) strains are valuable not only for detecting major gene segregation and linkage but also for identifying associations between behavior and quantitative trait loci (QTL) that account for relatively small amounts of variation in behaviors for which strain distribution patterns are not bimodal. When applied to published data on genetic markers and on behavior for BXD RI strains, the RI QTL association approach suggests the presence of QTLs on chromosomes 6 and 12 for open-field activity and on chromosomes 1, 2, and 17 for high-pressure seizure susceptibility. Because the RI QTL approach does not require that the progenitor inbred strains of a particular RI series differ, researchers could focus on the BXD RI series, for which the greatest number of genetic markers are available. Focusing on BXD would capitalize on the cumulative nature of RI research which permits analyses of QTL sources of genetic correlations across studies.	Plomin R, McClearn GE,ÊGora-Maslak G,Ê Neiderhiser JM.	Use of recombinant inbred strains to detect quantitative trait loci associated with behavior.	Behav Genet	277(2)	99-116	Mar	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2049054&dopt=Abstract	2049054	91264768	03	35-80 days	35	80			atm	89		71		89		89		71				83		83		74		77				83		83		71		89		86		83		89				83		74		77		74		83		89		74																												7/14/2003	MK Sullivan											2049054.03
Seizure susceptibility to high atmospheric pressure at 1000 atmospheres [measured at atm which seizure occurred]		Recombinant inbred (RI) strains are valuable not only for detecting major gene segregation and linkage but also for identifying associations between behavior and quantitative trait loci (QTL) that account for relatively small amounts of variation in behaviors for which strain distribution patterns are not bimodal. When applied to published data on genetic markers and on behavior for BXD RI strains, the RI QTL association approach suggests the presence of QTLs on chromosomes 6 and 12 for open-field activity and on chromosomes 1, 2, and 17 for high-pressure seizure susceptibility. Because the RI QTL approach does not require that the progenitor inbred strains of a particular RI series differ, researchers could focus on the BXD RI series, for which the greatest number of genetic markers are available. Focusing on BXD would capitalize on the cumulative nature of RI research which permits analyses of QTL sources of genetic correlations across studies.	Plomin R, McClearn GE,ÊGora-Maslak G,Ê Neiderhiser JM.	Use of recombinant inbred strains to detect quantitative trait loci associated with behavior.	Behav Genet	277(2)	99-116	Mar	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2049054&dopt=Abstract	2049054	91264768	04	35-80 days	35	80			atm	78		63		66		81		66				78		66		66		66				69		78		66		72		78		78		78				81		66		63		66		72		78		66																												7/14/2003	MK Sullivan											2049054.04
Sleep need; Slow wave sleep delta EEG power after 6 hrs sleep deprivation [%]		Delta power, a measure of EEG activity in the 1-4 Hz range, in slow-wave sleep (SWS) is in a quantitative and predictive relationship with prior wakefulness. Thus, sleep loss evokes a proportional increase in delta power, and excess sleep a decrease. Therefore, delta power is thought to reflect SWS need and its underlying homeostatically regulated recovery process. The neurophysiological substrate of this process is unknown and forward genetics might help elucidate the nature of what is depleted during wakefulness and recovered during SWS. We applied a mathematical method that quantifies the relationship between the sleep-wake distribution and delta power to sleep data of six inbred mouse strains. The results demonstrated that the rate at which SWS need accumulated varied greatly with genotype. This conclusion was confirmed in a "dose-response" study of sleep loss and changes in delta power; delta power strongly depended on both the duration of prior wakefulness and genotype. We followed the segregation of the rebound of delta power after sleep deprivation in 25 BXD recombinant inbred strains by quantitative trait loci (QTL) analysis. One "significant" QTL was identified on chromosome 13 that accounted for 49% of the genetic variance in this trait. Interestingly, the rate at which SWS need decreases did not vary with genotype in any of the 31 inbred strains studied. These results demonstrate, for the first time, that the increase of SWS need is under a strong genetic control, and they provide a basis for identifying genes underlying SWS homeostasis.	Franken P, Chollet D, Tafti M	The homeostatic regulation of sleep need is under genetic control.	J Neurosci 21:2610-2621	21(8)	2610-2621	Apr	2001	Paul Franken, Didier Chollet, and Mehdi Tafti The Homeostatic Regulation of Sleep Need Is under Genetic Control J. Neurosci. 2001 21: 2610-2621.	http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11306614&dopt=Abstract	11306614		01	67-142 days	67	142	Male	5	%	223.133	10.3	179.452	9.4	168.304	30.5	148.551	9.9	223.583	24.6	197.680	23.4	198.379	12.6	155.447	2.6	161.296	11.8	156.793	7.2	166.240	12.3	130.001	7.2	166.624	9.8	179.251	2.5			189.507	16.6	133.289	13.8	147.317	9.4	172.023	33.7	169.368	17.8	165.230	18.5	187.284	22.6	168.229	9.8	144.830	10.0	153.054	9.5	149.713	6.1	138.458	6.9	132.991	12.5																							6/5/2003	MK Sullivan	Rob Williams										11306614.01
Spiral ganglion cell density hook [cells per 10000 µm2]		The effects of three putative genes which contribute to age-related hearing loss (AHL genes) were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 25 recombinant BXD inbred mouse strains, originally derived from C57BL/6J (B6) and DBA/2J (D2) progenitor strains. All BXD strains showed substantial elevation of ABR thresholds and loss of spiral ganglion cells (SGCs) during the first year of life. The findings are consistent with our genetic model in which D2 and B6 inbred strains both possess the Ahl (age-related hearing loss) gene, whereas D2 possesses two additional chromosomal loci with AHL genes (Ahl2 and Ahl3). The between-strain distribution in the severity of SGC loss and ABR threshold elevations suggests that the severity of hearing loss is determined in large part by the number of AH L genes an animal possesses and by additional genetic background effects. The present findings also demonstrate that, because BXD strains vary substantially in the rate and severity of progressive hearing loss (but are genetically closely related), they can provide powerful animal models for developmental studies of AHL.	Willott JF, Erway LC	Genetics of age-related hearing loss in mice. IV. Cochlear pathology and hearing loss in 25 BXD recombinant inbred mouse strains.	Hear Res	119 (1-2)	27-36	May	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9641316&dopt=Abstract	9641316	98303018	01	1 year	365		MF		cells per 10000 µm2	17		8		17		4		9		8		4		8		8		7				10		7		3		8				5		6		7		9		6		18		3		12		12		9		12		6																								6/12/2003	MK Sullivan											9641316.01
Spiral ganglion cell density mid base [cells per 10000 µm2]		The effects of three putative genes which contribute to age-related hearing loss (AHL genes) were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 25 recombinant BXD inbred mouse strains, originally derived from C57BL/6J (B6) and DBA/2J (D2) progenitor strains. All BXD strains showed substantial elevation of ABR thresholds and loss of spiral ganglion cells (SGCs) during the first year of life. The findings are consistent with our genetic model in which D2 and B6 inbred strains both possess the Ahl (age-related hearing loss) gene, whereas D2 possesses two additional chromosomal loci with AHL genes (Ahl2 and Ahl3). The between-strain distribution in the severity of SGC loss and ABR threshold elevations suggests that the severity of hearing loss is determined in large part by the number of AH L genes an animal possesses and by additional genetic background effects. The present findings also demonstrate that, because BXD strains vary substantially in the rate and severity of progressive hearing loss (but are genetically closely related), they can provide powerful animal models for developmental studies of AHL.	Willott JF, Erway LC	Genetics of age-related hearing loss in mice. IV. Cochlear pathology and hearing loss in 25 BXD recombinant inbred mouse strains.	Hear Res	119 (1-2)	27-36	May	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9641316&dopt=Abstract	9641316	98303018	02	1 year	365		MF		cells per 10000 µm2	43		11		15		5		17		22		6		12		13		8				25		17		3		21				9		23		13		22		5		23		11		19		17		25		31		19																								6/12/2003	MK Sullivan											9641316.02
Spiral ganglion cell density mid-apical [cells per 10000 µm2]		The effects of three putative genes which contribute to age-related hearing loss (AHL genes) were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 25 recombinant BXD inbred mouse strains, originally derived from C57BL/6J (B6) and DBA/2J (D2) progenitor strains. All BXD strains showed substantial elevation of ABR thresholds and loss of spiral ganglion cells (SGCs) during the first year of life. The findings are consistent with our genetic model in which D2 and B6 inbred strains both possess the Ahl (age-related hearing loss) gene, whereas D2 possesses two additional chromosomal loci with AHL genes (Ahl2 and Ahl3). The between-strain distribution in the severity of SGC loss and ABR threshold elevations suggests that the severity of hearing loss is determined in large part by the number of AH L genes an animal possesses and by additional genetic background effects. The present findings also demonstrate that, because BXD strains vary substantially in the rate and severity of progressive hearing loss (but are genetically closely related), they can provide powerful animal models for developmental studies of AHL.	Willott JF, Erway LC	Genetics of age-related hearing loss in mice. IV. Cochlear pathology and hearing loss in 25 BXD recombinant inbred mouse strains.	Hear Res	119 (1-2)	27-36	May	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9641316&dopt=Abstract	9641316	98303018	03	1 year	365		MF		cells per 10000 µm2	46		25		40		15		16		25		11		33		28		12				26		21		4		22				26		23		21		25		20		27		10		29		23		24		35		32																								6/12/2003	MK Sullivan											9641316.03
Spiral ganglion cell density apical [cells per 10000 µm2]		The effects of three putative genes which contribute to age-related hearing loss (AHL genes) were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 25 recombinant BXD inbred mouse strains, originally derived from C57BL/6J (B6) and DBA/2J (D2) progenitor strains. All BXD strains showed substantial elevation of ABR thresholds and loss of spiral ganglion cells (SGCs) during the first year of life. The findings are consistent with our genetic model in which D2 and B6 inbred strains both possess the Ahl (age-related hearing loss) gene, whereas D2 possesses two additional chromosomal loci with AHL genes (Ahl2 and Ahl3). The between-strain distribution in the severity of SGC loss and ABR threshold elevations suggests that the severity of hearing loss is determined in large part by the number of AH L genes an animal possesses and by additional genetic background effects. The present findings also demonstrate that, because BXD strains vary substantially in the rate and severity of progressive hearing loss (but are genetically closely related), they can provide powerful animal models for developmental studies of AHL.	Willott JF, Erway LC	Genetics of age-related hearing loss in mice. IV. Cochlear pathology and hearing loss in 25 BXD recombinant inbred mouse strains.	Hear Res	119 (1-2)	27-36	May	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9641316&dopt=Abstract	9641316	98303018	04	1 year	365		MF		cells per 10000 µm2	47		24		27		25		20		30		35		26		18		21				20		19		12		16				16		32		18		22		32		30		11		14		10		4		19		33																								6/12/2003	MK Sullivan											9641316.04
Spiral ganglion cell density total [cells per 10000 µm2]		The effects of three putative genes which contribute to age-related hearing loss (AHL genes) were evaluated using auditory brainstem response (ABR) thresholds and post-mortem cochlear histopathology in 25 recombinant BXD inbred mouse strains, originally derived from C57BL/6J (B6) and DBA/2J (D2) progenitor strains. All BXD strains showed substantial elevation of ABR thresholds and loss of spiral ganglion cells (SGCs) during the first year of life. The findings are consistent with our genetic model in which D2 and B6 inbred strains both possess the Ahl (age-related hearing loss) gene, whereas D2 possesses two additional chromosomal loci with AHL genes (Ahl2 and Ahl3). The between-strain distribution in the severity of SGC loss and ABR threshold elevations suggests that the severity of hearing loss is determined in large part by the number of AH L genes an animal possesses and by additional genetic background effects. The present findings also demonstrate that, because BXD strains vary substantially in the rate and severity of progressive hearing loss (but are genetically closely related), they can provide powerful animal models for developmental studies of AHL.	Willott JF, Erway LC	Genetics of age-related hearing loss in mice. IV. Cochlear pathology and hearing loss in 25 BXD recombinant inbred mouse strains.	Hear Res	119 (1-2)	27-36	May	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9641316&dopt=Abstract	9641316	98303018	05	1 year	365		MF		cells per 10000 µm2	168		68		100		49		62		85		56		79		67		48				81		64		22		67				56		84		59		78		53		98		35		74		62		62		97		90																								6/12/2003	MK Sullivan											9641316.05
Stem cell frequency, CAFC day 35/100000 cells		We evaluated in vivo interactions between extrinsic (growth factor induced) and intrinsic (genetically determined) effectors of mouse primitive hemopoietic stem cell proliferation and numbers. Accordingly, stem cell frequency and cell cycle kinetics were assessed in eight strains of inbred mice using the cobblestone area-forming cell (CAFC) assay. A strong inverse correlation was observed between mouse lifespan and the number of autonomously cycling progenitors (CAFC day 7) in the femur. The population size of primitive stem cells (CAFC day 35) varied widely (up to sevenfold) among strains, unlike total CAFC day 7 numbers (cycling and quiescent), which were similar. Administration of the early acting cytokine flt-3 ligand to these strains resulted in activation of quiescent primitive stem cells exclusively in strains with high endogenous stem cell numbers (DBA and AKR), but was unrelated to strain-specific progenitor cell cycling. To map loci affecting stem cell frequency, we quantified stem cells in BXD recombinant inbred mice (offspring of C57BL/6 and DBA/2). The resulting strain distribution pattern showed high concordance with a marker that mapped to chromosome 18 (19 cM). Linkage with this genomic interval was associated with a likelihood of odds score of 3.3, surpassing the level required for significance. Interestingly, this segment, containing the EGR-1 gene, shows synteny with human chromosome 5q, a region strongly associated with various hematological malignancies. Our findings indicate that a gene mapping to this region is mutated in either C57BL/6 or DBA/2 (and possibly AKR) mice. These studies in apparently healthy mice may facilitate the identification of a gene implicated in human 5q-syndromes.	de Haan G, Van Zant G.	Intrinsic and extrinsic control of hemopoietic stem cell numbers: mapping of a stem cell gene.	J Exp Med	186(4)	529-536	Aug	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9254651&dopt=Abstract	9254651		01	6-8 wks	42	56	Female	3	CAFC day 35/100000 cells	1.2		3.3		1.0		3.4		2.9		1.6		2.1		3.5		8.22		1.6		0.9		2.6		2.1		2.4		2.3		2.1		1.9		2.2		2.2		1.8		1.8		1.2		1.8		2.5		.5		2.5		2.8		2.9																								12/30/2002		Nathan Copeland										9254651.01
Striatum cholinergic neurons section 11 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	01	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	60	5	86	4	72	4	75	4	80	2	69	4	92	7	80	4	73	2	52	5	74	2	66	4	70	4	64	3	68	2	93	7	86	5	71	4	85	4	68	4	99	5	96	6			80	3	62	3	72	1	75	5	95	5																							6/22/2003	MK Sullivan											8968368.01
Striatum cholinergic neurons section 14 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	02	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	91	5	116	3	104	4	103	3	103	4	117	4	122	4	124	3	115	3	89	2	101	4	94	4	93	4	86	7	132	3	129	5	139	3	110	4	111	6	93	3	111	6	139	4			130	5	97	4	97	3	109	4	145	5																							6/22/2003	MK Sullivan											8968368.02
Striatum cholinergic neurons section 17 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	03	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	110	4	135	2	133	4	117	3	124	6	130	4	174	7	142	4	138	4	125	7	127	4	131	7	117	6	127	6	174	6	161	9	159	5	127	1	129	6	130	6	156	7	166	9			140	2	148	5	137	5	139	2	152	5																							6/22/2003	MK Sullivan											8968368.03
Striatum cholinergic neurons section 20 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	04	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	105	3	134	5	109	2	106	3	115	6	125	5	135	5	132	3	125	4	117	6	123	4	136	4	116	3	133	5	134	4	153	7	143	5	122	2	135	6	120	5	138	7	156	5			116	4	142	3	117	3	124	4	137	6																							6/22/2003	MK Sullivan											8968368.04
Striatum cholinergic neurons section 22 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	05	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	70	3	89	4	76	3	67	3	62	3	75	2	97	8	82	3	95	5	72	3	60	2	72	4	65	4	70	5	75	5	71	3	76	6	66	4	82	5	76	1	83	3	85	3			70	2	102	3	74	2	87	2	85	6																							6/22/2003	MK Sullivan											8968368.05
Striatum cholinergic neurons section 24 [number of neurons]		Compared with the neuroleptic nonresponsive (NNR) mouse line, the neuroleptic responsive (NR) line has a significantly higher number of striatal cholinergic neurons (Hitzemann et al., 1993). We now report additional information on this genetic association. At the fifth selected generation, a new selection of the NR and NNR lines differed 5-fold in their ED50 values (1 vs. 5 mg/kg) for haloperidol-induced catalepsy and 20% in the number of striatal cholinergic neurons (higher in the NR line). This association was further examined in 10 standard inbred mouse strains; eight of the strains had been crossed to form the heterogeneous stock from which the new NR and NNR lines were selected. In this panel, we detected no significant association between number of cholinergic neurons and haloperidol response. To examine the similarities and differences in the modes of inheritance for the two phenotypes, we formed a full Mendelian cross from the C57BL/6 (B6) and DBA/2 (D2) mouse strains. The B6 and D2 strains differ 9-fold in their haloperidol ED50 values (3.9 vs. 0.4 mg/kg) and more than 30% in the number of cholinergic neurons (higher in the D2 strain). Haloperidol-induced catalepsy was described by a simple additive genetic model; the narrow sense heritability was 0.60. In contrast, for the number of cholinergic neurons, the B6 genotype was dominant and heterosis was detected in the F1 cross. Despite the differences in heritability, among B6D2 F2 individuals, increasing haloperidol sensitivity was associated with increasing numbers of striatal cholinergic neurons. The BXD recombinant inbred series (25 strains) showed a 16-fold range of variation in the haloperidol ED50 and a greater than 50% variation in the number of striatal cholinergic neurons. However, we detected no significant association between haloperidol response and number of cholinergic neurons. Overall, the data suggest that the genetic association between the phenotypes is modest, complex and detectable only with some genetic strategies.	Dains K, Hitzemann B	Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum.	J Pharmacol Exp Ther	279(3)	1430-1438	Dec	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8968368&dopt=Abstract	8968368	97123119	06	8-10 wks	56	70	Male 	9-12	Number of striatal cholinergic neurons	47	2	67	3	40	2	52	2	51	1	49	1	48	3	44	2	52	2	46	2	47	3	44	1	42	2	48	5	46	3	62	3	46	1	47	3	53	2	44	2	52	3	51	2			44	2	61	2	45	2	58	3	54	3	                      																						6/22/2003	MK Sullivan											8968368.06
Hippocampus bilateral weight [mg]		Notable differences in hippocampal structure are associated with intriguing differences in development and behavioral capabilities. We explored genetic and environmental factors that modulate hippocampal size, structure, and cell number using sets of C57BL/6J (B6) and DBA/2J (D2) mice; their F1 and F2 intercrosses (n = 180); and 35 lines of BXD recombinant inbred (RI) strains. Hippocampal weights of the parental strains differ by 20%. Estimates of granule cell number also differ by approximately 20%. Hippocampal weights of RI strains range from 21 to 31 mg, and those of individual F2 mice range from 23 to 36 mg (bilateral weights). Volume and granule cell number are well correlated (r = 0.7-0.8). Significant variation is associated with differences in age and sex. The hippocampus increases in weight by 0.24 mg per month, and those of males are 0.55 mg heavier (bilateral) than those of females. Heritability of variation is approximately 50%, and half of this genetic variation is generated by two quantitative trait loci that map to chromosome 1 (Hipp1a: genome-wide p < 0.005, between 65 and 100 cM) and to chromosome 5 (Hipp5a, p < 0.05, between 15 and 40 cM). These are among the first gene loci known to produce normal variation in forebrain structure. Hipp1a and Hipp5a individually modulate hippocampal weight by 1.0-2.0 mg, an effect size greater than that generated by age or sex. The Hipp gene loci modulate neuron number in the dentate gyrus, collectively shifting the population up or down by as much as 200,000 cells. Candidate genes for the Hipp loci include Rxrg and Fgfr3.	Lu L, Airey DC, Williams RW	Complex trait analysis of the hippocampus: mapping and biometric analysis of two novel gene loci with specific effects on hippocampal structure in mice.	J Neurosci	21(10)	3503-3514	May	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331379&dopt=Abstract	11331379		02	~ 80 days			MF		mg	28.4		23.0		27.6		24.9		29.9		26.7		28.7		25.7		25.2		26.7		23.5		26.4		26.2		28.1		26.0		28.0		24.3		25.6		24.5		24.5		21.6		23.7		22.9		24.1		23.3		21.3		23.7		24.1		26.7		24.4		26.4		26.4		23.6		28.3		25.3		30.8				27.5				7/23/2003	MK Sullivan	Nathan Copeland										11331379.02
Hippocampus granule cell density per mm3 [x103]		Notable differences in hippocampal structure are associated with intriguing differences in development and behavioral capabilities. We explored genetic and environmental factors that modulate hippocampal size, structure, and cell number using sets of C57BL/6J (B6) and DBA/2J (D2) mice; their F1 and F2 intercrosses (n = 180); and 35 lines of BXD recombinant inbred (RI) strains. Hippocampal weights of the parental strains differ by 20%. Estimates of granule cell number also differ by approximately 20%. Hippocampal weights of RI strains range from 21 to 31 mg, and those of individual F2 mice range from 23 to 36 mg (bilateral weights). Volume and granule cell number are well correlated (r = 0.7-0.8). Significant variation is associated with differences in age and sex. The hippocampus increases in weight by 0.24 mg per month, and those of males are 0.55 mg heavier (bilateral) than those of females. Heritability of variation is approximately 50%, and half of this genetic variation is generated by two quantitative trait loci that map to chromosome 1 (Hipp1a: genome-wide p < 0.005, between 65 and 100 cM) and to chromosome 5 (Hipp5a, p < 0.05, between 15 and 40 cM). These are among the first gene loci known to produce normal variation in forebrain structure. Hipp1a and Hipp5a individually modulate hippocampal weight by 1.0-2.0 mg, an effect size greater than that generated by age or sex. The Hipp gene loci modulate neuron number in the dentate gyrus, collectively shifting the population up or down by as much as 200,000 cells. Candidate genes for the Hipp loci include Rxrg and Fgfr3.	Lu L, Airey DC, Williams RW	Complex trait analysis of the hippocampus: mapping and biometric analysis of two novel gene loci with specific effects on hippocampal structure in mice.	J Neurosci	21(10)	3503-3514	May	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331379&dopt=Abstract	11331379		03	~ 80 days			MF		x103	857		871		1040		849		859				974		936		756		985		850		880		907		892		1010		954		921				928		828		1053		782		837		932		900		905		860		970		822		850		897		837				793		793		853				748				7/23/2003	MK Sullivan	Nathan Copeland										11331379.03
Brain weight [mg]		Notable differences in hippocampal structure are associated with intriguing differences in development and behavioral capabilities. We explored genetic and environmental factors that modulate hippocampal size, structure, and cell number using sets of C57BL/6J (B6) and DBA/2J (D2) mice; their F1 and F2 intercrosses (n = 180); and 35 lines of BXD recombinant inbred (RI) strains. Hippocampal weights of the parental strains differ by 20%. Estimates of granule cell number also differ by approximately 20%. Hippocampal weights of RI strains range from 21 to 31 mg, and those of individual F2 mice range from 23 to 36 mg (bilateral weights). Volume and granule cell number are well correlated (r = 0.7-0.8). Significant variation is associated with differences in age and sex. The hippocampus increases in weight by 0.24 mg per month, and those of males are 0.55 mg heavier (bilateral) than those of females. Heritability of variation is approximately 50%, and half of this genetic variation is generated by two quantitative trait loci that map to chromosome 1 (Hipp1a: genome-wide p < 0.005, between 65 and 100 cM) and to chromosome 5 (Hipp5a, p < 0.05, between 15 and 40 cM). These are among the first gene loci known to produce normal variation in forebrain structure. Hipp1a and Hipp5a individually modulate hippocampal weight by 1.0-2.0 mg, an effect size greater than that generated by age or sex. The Hipp gene loci modulate neuron number in the dentate gyrus, collectively shifting the population up or down by as much as 200,000 cells. Candidate genes for the Hipp loci include Rxrg and Fgfr3.	Lu L, Airey DC, Williams RW	Complex trait analysis of the hippocampus: mapping and biometric analysis of two novel gene loci with specific effects on hippocampal structure in mice.	J Neurosci	21(10)	3503-3514	May	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331379&dopt=Abstract	11331379		04	~ 80 days			MF		mg	496		415		433		417		544		386		477		448		415		453		384		412		447		455		435		436		399		429		441		435		388		412		373		415		403		367		409		444		427		420		413		405		411		418		405		438				443				7/23/2003	MK Sullivan	Nathan Copeland										11331379.04
Hippocampus granule cell number [x103]		Notable differences in hippocampal structure are associated with intriguing differences in development and behavioral capabilities. We explored genetic and environmental factors that modulate hippocampal size, structure, and cell number using sets of C57BL/6J (B6) and DBA/2J (D2) mice; their F1 and F2 intercrosses (n = 180); and 35 lines of BXD recombinant inbred (RI) strains. Hippocampal weights of the parental strains differ by 20%. Estimates of granule cell number also differ by approximately 20%. Hippocampal weights of RI strains range from 21 to 31 mg, and those of individual F2 mice range from 23 to 36 mg (bilateral weights). Volume and granule cell number are well correlated (r = 0.7-0.8). Significant variation is associated with differences in age and sex. The hippocampus increases in weight by 0.24 mg per month, and those of males are 0.55 mg heavier (bilateral) than those of females. Heritability of variation is approximately 50%, and half of this genetic variation is generated by two quantitative trait loci that map to chromosome 1 (Hipp1a: genome-wide p < 0.005, between 65 and 100 cM) and to chromosome 5 (Hipp5a, p < 0.05, between 15 and 40 cM). These are among the first gene loci known to produce normal variation in forebrain structure. Hipp1a and Hipp5a individually modulate hippocampal weight by 1.0-2.0 mg, an effect size greater than that generated by age or sex. The Hipp gene loci modulate neuron number in the dentate gyrus, collectively shifting the population up or down by as much as 200,000 cells. Candidate genes for the Hipp loci include Rxrg and Fgfr3.	Lu L, Airey DC, Williams RW	Complex trait analysis of the hippocampus: mapping and biometric analysis of two novel gene loci with specific effects on hippocampal structure in mice.	J Neurosci	21(10)	3503-3514	May	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331379&dopt=Abstract	11331379		05	~ 80 days			MF		x103	886		697		1067		639		835				1155		708		793		887		864		1019		766				800		1002		709				960		725		766		966		684		742		645		734		700		809		760		533		772		664				718		776		995				794				7/23/2003	MK Sullivan	Nathan Copeland										11331379.05
Testicular weight [g] 		Testicular weights were studied in the mouse BXD recombinant inbred (RI) strains. These strains were derived from DBA/2J and C57BL/6J progenitors that differ significantly in their testicular weights (0.224 g +/- 0.015 vs. 0.161 g +/- 0.03, P < 0.0001). The heritability of testicular weights was calculated to be 0.53, and the minimum number of responsible effective factors was estimated to be 5.7. The total genome scanning of the BXD RI strains with over 1000 markers revealed a quantitative trait locus (QTL) on mouse Chromosome (Chr) 13 near the D13Mit3 marker (LOD score 6.9). This QTL region was designated Twq1 and associated with over 75% of genetic variability.	Zidek V, Musilova A, Pintir J, Simakova M, Pravenec M.	Genetic dissection of testicular weight in the mouse with the BXD recombinant inbred strains.	Mamm Genome	9(7)	503-505	Jul	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9657844&dopt=Abstract	9657844	98325598	01	11 wks	77		Male	4-9	g	0.16	0.040	0.22	0.030	0.16	0.016	0.22	0.014	0.22	0.050	0.23	0.010	0.17	0.007			0.21	0.034	0.16	0.043	0.13	0.010	0.16	0.007	0.24	0.037	0.24	0.023	0.15	0.008	0.14	0.017			0.20	0.017	0.25	0.016	0.14	0.018	0.24	0.008	0.16	0.007	0.16	0.014	0.21	0.016	0.17	0.009	0.16	0.010	0.16	0.010	0.20	0.012																							7/14/2003	MK Sullivan											9657844.01
Tolerance delta to ethanol induced ataxia - maximal threshold minus onset threshold		Rapid tolerance to rotarod ataxia has previously been demonstrated in mice after sequential ethanol injections. Here we tested DBA/2J and C57BL/6J mice for initial ethanol sensitivity; DBA/2J mice were more sensitive (0.40 +/- 0.17 mg/g brain) than C57BL/6J mice (1.44 +/- 0.12 mg/g). We then monitored the development of tolerance by quantifying blood ethanol concentrations at the recovery from ataxia over five sequential injections; tolerance reached a plateau in about 5 hr. DBA/2J mice became very tolerant (final ethanol threshold 3.47 +/- 0.16 mg/ml, an increase of 3.07 mg/ml, or 8.7-fold above base line); B6 became slightly tolerant (final ethanol threshold 2.62 +/- 12 mg/ml, and increase of 1.18, or 1.8-fold above base line). Therefore, by the end of the treatment regimen, the rank order of sensitivity of the two strains had reversed. We then tested 25 recombinant inbred strains from among strains representing a cross between C57BL/6J and DBA/2J inbred strains, followed by a quantitative trait locus analysis with a database of 1522 markers to identify provisional loci. This procedure identified 19 markers on 11 chromosomes for initial sensitivity, 18 markers on 9 chromosomes for tolerance (delta) and 21 markers on 11 chromosomes for tolerance (fold-increase). Of these, 17 markers were in common, which suggests that initial sensitivity and tolerance share substantial genetic codetermination. Major candidate loci will be confirmed by genotyping B6D2F2 offspring that have been tested for initial sensitivity and tolerance.	Gallaher EJ, Jones GE	Mapping the genes for haloperidol-induced catalepsy.	J Pharmacol Exp Ther	277(2)	604-612	May	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627537&dopt=Abstract	8627537	96210104	03	44-135 days	44	135	Male			1.18		3.07		2.54		1.85		1.95		1.19		2.36		2.47		2.36		1.69		2.56		1.85		2.25		1.66		1.58		1.83				1.86		2.79		2.22		2.54		2.1		1.87		2.52		1.54		2.49		1.42		3.05																								12/19/2002												8627537.03
Tolerance fold-increase to ethanol induced ataxia - maximal threshold divided by onset threshold		Rapid tolerance to rotarod ataxia has previously been demonstrated in mice after sequential ethanol injections. Here we tested DBA/2J and C57BL/6J mice for initial ethanol sensitivity; DBA/2J mice were more sensitive (0.40 +/- 0.17 mg/g brain) than C57BL/6J mice (1.44 +/- 0.12 mg/g). We then monitored the development of tolerance by quantifying blood ethanol concentrations at the recovery from ataxia over five sequential injections; tolerance reached a plateau in about 5 hr. DBA/2J mice became very tolerant (final ethanol threshold 3.47 +/- 0.16 mg/ml, an increase of 3.07 mg/ml, or 8.7-fold above base line); B6 became slightly tolerant (final ethanol threshold 2.62 +/- 12 mg/ml, and increase of 1.18, or 1.8-fold above base line). Therefore, by the end of the treatment regimen, the rank order of sensitivity of the two strains had reversed. We then tested 25 recombinant inbred strains from among strains representing a cross between C57BL/6J and DBA/2J inbred strains, followed by a quantitative trait locus analysis with a database of 1522 markers to identify provisional loci. This procedure identified 19 markers on 11 chromosomes for initial sensitivity, 18 markers on 9 chromosomes for tolerance (delta) and 21 markers on 11 chromosomes for tolerance (fold-increase). Of these, 17 markers were in common, which suggests that initial sensitivity and tolerance share substantial genetic codetermination. Major candidate loci will be confirmed by genotyping B6D2F2 offspring that have been tested for initial sensitivity and tolerance.	Gallaher EJ, Jones GE	Mapping the genes for haloperidol-induced catalepsy.	J Pharmacol Exp Ther	277(2)	604-612	May	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8627537&dopt=Abstract	8627537	96210104	04	44-135 days	44	135	Male			1.82		8.68		3.1		2.7		3.44		2.16		4.06		3.13		3.68		2.8		4.61		3.31		6.49		2.36		2.23		2.87				2.74		6.69		3.47		4.53		2.96		3.34		4.65		2.12		3.42		2.23		7.93																								12/19/2002												8627537.04
Saccharin Preference vs Water Ratio [%]		The sac locus, with a major effect on saccharin preference, was discovered by Fuller (1974) in C57BL/6J (B6), DBA/2J (D2), and derived crosses, and is now supported in the BXD/Ty recombinant inbred (RI) series by a marked bimodal distribution in saccharin preference among 20 strains. The B6 allele led to increased saccharin preference compared to the D2 allele. Since the search for bimodal distributions reflecting major gene loci is an essential part of RI strain analysis, a new statistical method is proposed to test for bimodality, and comparisons are made to previously proposed methods. Another new RI method, quantitative trait loci (QTL) analysis, allows provisional detection and mapping of minor as well as major gene loci. Using this method as a screen, significant associations with saccharin preference were suggested with marker loci on portions of six chromosomes. One of these, the D12nyu1 locus on chromosome 12, was independently supported in a panel of standard (non-RI) inbred strains also tested for saccharin preference. It is unclear whether this reflects the sac locus.	Belknap JK, Crabbe JC, Plomin R, McClearn GE, Sampson KE, O'Toole LA, Gora-Maslak G.	Single-locus control of saccharin intake in BXD/Ty recombinant inbred (RI) mice: some methodological implications for RI strain analysis	Behav Genet	22(1)	81-100	Jan	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1590732&dopt=Abstract	1590732		01	8-12 wks	56	84	Male	4-8	%	96	1	59	10	74	4	82	7	90	5	91	1	57	11	60	12			77	6	57	8	85	8	82	8	86	1	77	10					61	14	61	14	79	8	91	2	64	16	76	9	87	4	83	5																													6/25/2003	MK Sullivan											1590732.01
Saccharin Consumption [mg/kg/day]		The sac locus, with a major effect on saccharin preference, was discovered by Fuller (1974) in C57BL/6J (B6), DBA/2J (D2), and derived crosses, and is now supported in the BXD/Ty recombinant inbred (RI) series by a marked bimodal distribution in saccharin preference among 20 strains. The B6 allele led to increased saccharin preference compared to the D2 allele. Since the search for bimodal distributions reflecting major gene loci is an essential part of RI strain analysis, a new statistical method is proposed to test for bimodality, and comparisons are made to previously proposed methods. Another new RI method, quantitative trait loci (QTL) analysis, allows provisional detection and mapping of minor as well as major gene loci. Using this method as a screen, significant associations with saccharin preference were suggested with marker loci on portions of six chromosomes. One of these, the D12nyu1 locus on chromosome 12, was independently supported in a panel of standard (non-RI) inbred strains also tested for saccharin preference. It is unclear whether this reflects the sac locus.	Belknap JK, Crabbe JC, Plomin R, McClearn GE, Sampson KE, O'Toole LA, Gora-Maslak G.	Single-locus control of saccharin intake in BXD/Ty recombinant inbred (RI) mice: some methodological implications for RI strain analysis	Behav Genet	22(1)	81-100	Jan	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1590732&dopt=Abstract	1590732		02	8-12 wks	56	84	Male	4-8	mg/kg/day	677	20	294	47	333	19	473	53	1228	186	519	34	267	55	286	68			475	33	253	51	601	63	457	58	458	31	436	53					354	101	264	61	380	41	500	51	477	142	358	80	469	36	450	36																													6/25/2003	MK Sullivan											1590732.02
Parity distribution of MMTV virus-specific RNA (Primiparous) [%]		The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences.	Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC.	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	Genetics	111(3)	597-615	Nov	1985		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2996982&dopt=Abstract	2996982		01	3-9 months	90	270	Female		%	0.0265	0.0091	0.0160	0.0001	0.0216	0.0070	0.0062	0.0029	0.0230	0.0100	0.0192	0.0066	0.0138	0.0100	0.0064	0.0021	0.0141	0.0040	0.0120	0.0041	0.0149	0.0013	0	0	0.0134	0.0076	0.0067	0.0018	0.0118	0.0058	0.0198	0.0067			0.0062	0.0019	0.0030	0.0011	0.0160	0.0001	0.0107	0.0051	0.0268	0.0072			0.0077	0.0037	0.0198	0.0067	0.0190	0.0084	0.0267	0.0092	0.0240	0.0092																							6/25/2003	MK Sullivan											2996982.01
Parity distribution of MMTV virus-specific RNA (Multiparous) [%]		The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences.	Traina-Dorge VL, Carr JK, Bailey-Wilson JE, Elston RC, Taylor BA, Cohen JC.	Cellular genes in the mouse regulate in trans the expression of endogenous mouse mammary tumor viruses.	Genetics	111(3)	597-615	Nov	1985		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2996982&dopt=Abstract	2996982		02	3-9 months	90	270	Female		%	0.024	0.0090			0.032	0	0.0077	0.0029	0.028	0.0068	0.0212	0.0091	0.0161	0			0.0213	0.0083	0.0213	0.0083	0.0240	0.0112	0.0034	0.0021			0.0252	0.0081	0.0161	0	0.0214	0.0067			0.0064	0.0019	0.0160	0	0.0133	0.0040	0.0240	0.0072					0.0184	0.0051	0.0230	0.0076	0.0160	0	0.0160	0	0.0310	0.0190																							6/25/2003	MK Sullivan											2996982.02
Morphine analgesia in response to 16 mg/kg morphine [%MPE]		A quantitative trait locus (QTL) was detected and mapped to proximal chromosome 10 near the markers Mpmv5 and D10Mit51 with a strong influence on morphine-induced analgesia in the BXD recombinant inbred (RI) strains and in an F2 cross (B6D2F2) between the BXD progenitor strains, C57BL/6 and DBA/2. A LOD score of 3.9 (p < .00002) was seen for analgesia using the hot plate assay. Naloxone Bmax was also associated with this chromosome region in BXD RI mice. The mu opioid receptor gene (Oprm) has recently been mapped to this same chromosome region. The observation that several morphine-related traits and naloxone Bmax appear to be partly determined by this presumed single locus is consistent with the hypothesis that the mu opioid receptor gene, or one of its modulators, is the basis for the QTL.	Belknap JK, Mogil JS, Helms ML, Richards SP, O'Toole LA, Bergeson SE, Buck KJ.	Localization to chromosome 10 of a locus influencing morphine analgesia in crosses derived from C57BL/6 and DBA/2 strains.	Life Sci	57(10)	PL117-PL124	Oct	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7643715&dopt=Abstract	7643715		01	100 days	100		Male	8	% MPE	13	2.2	82	11.7	63	5.6	73	8.8	45	7.8	16	5.4	72	6.3	50	10.9			10	2.7	20	2.3	23	8.2	32	6.9	25	9.8	33	8.2					18	1.6	12	2.2	60	9.6	80	7.1	30	9.0	55	8.8	45	5.8	18	0.7																													6/11/2003	MK Sullivan											7643715.01
[3H]-naloxone Bmax [pM]		A quantitative trait locus (QTL) was detected and mapped to proximal chromosome 10 near the markers Mpmv5 and D10Mit51 with a strong influence on morphine-induced analgesia in the BXD recombinant inbred (RI) strains and in an F2 cross (B6D2F2) between the BXD progenitor strains, C57BL/6 and DBA/2. A LOD score of 3.9 (p < .00002) was seen for analgesia using the hot plate assay. Naloxone Bmax was also associated with this chromosome region in BXD RI mice. The mu opioid receptor gene (Oprm) has recently been mapped to this same chromosome region. The observation that several morphine-related traits and naloxone Bmax appear to be partly determined by this presumed single locus is consistent with the hypothesis that the mu opioid receptor gene, or one of its modulators, is the basis for the QTL.	Belknap JK, Mogil JS, Helms ML, Richards SP, O'Toole LA, Bergeson SE, Buck KJ.	Localization to chromosome 10 of a locus influencing morphine analgesia in crosses derived from C57BL/6 and DBA/2 strains.	Life Sci	57(10)	PL117-PL124	Oct	1995		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7643715&dopt=Abstract	7643715		02	100 days	100		Male	6	pM	84	1.9	95	2.6			104	7.1	90	9.2	92	7.1	95	2.6	100	0.7			90	9.7	90	1.8	83	5.0			76	4.0	84	4.7					83	2.8	74	1.7	88	8.2	86	5.3	92	4.0	90	3.7	103	3.5	86	1.8																													6/11/2003	MK Sullivan											7643715.02
Ethanol withdrawal handling induced convulsions, 2 - 12 hours after 4 g/kg 20% v/v EtOH, Area Under Curve		Alcohol dependence (alcoholism) is accompanied by evidence of tolerance, withdrawal (physiological dependence), or compulsive behavior related to alcohol use. Studies of strain and individual differences using animal models for acute physiological dependence liability are useful means to identify potential genetic determinants of liability in humans. Behavioral and quantitative trait analyses were conducted using animal models for high risk versus resistance to acute physiological dependence. Using a two-step genetic mapping strategy, loci on mouse chromosomes 1,æ4,æand 11æwere mapped that contain genes that influence alcohol withdrawal severity. In the aggregate, these three risk markers accounted for 68% of the genetic variability in alcohol withdrawal. Candidate genes in proximity to the chromosome 11ælocus include genes encoding the 1, 6, and 2 subunits of type-A receptors for the inhibitory neurotransmitter, GABA. In addition, suggestive linkage is indicated for two loci on mouse chromosome 2,æone near Gad1 encoding glutamic acid decarboxylase, and the other near the El2 locus which influences the seizure phenotype in the neurological mutant strain El. The present analyses detect and map some of the loci that increase risk to develop physiological dependence and may facilitate identification of genes related to the development of alcoholism. Syntenic conservation between human and mouse chromosomes suggests that human homologs of genes that increase risk for physiological dependence may localize to 1q21-q32, 2q24-q37/11p13, 9p21-p23/1p32-p22.1, and 5q32-q35.	Buck KJ, Metten P, Belknap JK, Crabbe JC.	Quantitative Trait Loci Involved in Genetic Predisposition to Acute Alcohol Withdrawal in Mice	J Neurosci 	17(10)	3946-3955	May	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9133412&dopt=Abstract	9133412		01	8-15 wks	56 	105	MF			6.8		15.5		14.5		13		14.2		2.7		7.9		18.7				5		16.4		10.4		4.3		7		4.5						9.3		9.8				2.5		6.4		11.1		6.7		1.5				0		6.4																								6/11/2003	MK Sullivan											9133412.01
Baseline handling induced convulsions		Alcohol dependence (alcoholism) is accompanied by evidence of tolerance, withdrawal (physiological dependence), or compulsive behavior related to alcohol use. Studies of strain and individual differences using animal models for acute physiological dependence liability are useful means to identify potential genetic determinants of liability in humans. Behavioral and quantitative trait analyses were conducted using animal models for high risk versus resistance to acute physiological dependence. Using a two-step genetic mapping strategy, loci on mouse chromosomes 1,æ4,æand 11æwere mapped that contain genes that influence alcohol withdrawal severity. In the aggregate, these three risk markers accounted for 68% of the genetic variability in alcohol withdrawal. Candidate genes in proximity to the chromosome 11ælocus include genes encoding the 1, 6, and 2 subunits of type-A receptors for the inhibitory neurotransmitter, GABA. In addition, suggestive linkage is indicated for two loci on mouse chromosome 2,æone near Gad1 encoding glutamic acid decarboxylase, and the other near the El2 locus which influences the seizure phenotype in the neurological mutant strain El. The present analyses detect and map some of the loci that increase risk to develop physiological dependence and may facilitate identification of genes related to the development of alcoholism. Syntenic conservation between human and mouse chromosomes suggests that human homologs of genes that increase risk for physiological dependence may localize to 1q21-q32, 2q24-q37/11p13, 9p21-p23/1p32-p22.1, and 5q32-q35.	Buck KJ, Metten P, Belknap JK, Crabbe JC.	Quantitative Trait Loci Involved in Genetic Predisposition to Acute Alcohol Withdrawal in Mice	J Neurosci 	17(10)	3946-3955	May	1997		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9133412&dopt=Abstract	9133412		02	8-15 wks	56	105	MF			0.93		0.45		1.87		1.81		1.25		0.44		1.17		1.85				5.2		1.59		1.91		0.13		0.67		5						0.64		0.69				0.19		00.24		1.78		0.89		0.15				0		5																								6/11/2003	MK Sullivan											9133412.02
BCG induced anergy (delayed type hypersensitivity)-footpad swelling in response to BCG [mm]		We previously reported that BCG-induced anergy in mice (evaluated by delayed hypersensitivity to sheep erythrocytes) is unigenic and influenced by genes linked to the immunoglobulin heavy chain allotype (Igh). Using congenic mice (either H-2k or H-2b), we could not detect H-2-linked control of anergy. The current study re-examines this issue by using both BXD (H-2b or H-2d) and BXH (H-2b or H-2k) recombinant inbred (RI) mice as well as H-2 recombinant mice of different haplotypes. BXD RI (H-2b) mice were more anergic than BXD RI (H-2d) animals. Also, BXD RI (Ighb animals were more anergic than BXD RI (Ighc) mice. By evaluating combinations of H-2 haplotypes and Igh allotypes, we found the most anergic animals to be H-2b, Ighb. BCG-induced anergy then appears to be influenced by genes linked to both the H-2 and Igh complexes. BCG-induced anergy developed in H-2 recombinant mice (C57BL/10 background) that were either H-2b or H-2k, but not in H-2d animals. Experiments in the B10.A mouse suggested that genes within the H-2K through H-2I were influential. A more definitive map is presented of Igh-linked genes influencing anergy, suggesting that these genes are approximately 23 recombination units on the centromeric side of Igh-1 between Igh-Src and Lyb-7.	Callis AH, Schrier DJ, David CS, Moore VL.	Immunogenetics of BCG-induced anergy in mice. Control by Igh- and H-2-linked genes.	Immunology	49(4)	609-615	Aug	1983		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6409803&dopt=Abstract	6409803		01	8-12 wks	56	84	Female except BXD RI	2-14	mm							.22	0.08					0.14	0.03					0.79	0.04	0.79	0.21	0.15	0.05	.48	0.14					0.15	0.03	0.86	0.08					0.3	0.12									0.24	0.08																													6/9/2003	MK Sullivn											6409803.01
Ethanol induced ataxia - initial sensitivity  Blood ethanol concentrations (BECo) at loss of balance on dowel test [mg %]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		01	55-80 days	55	80	Male	6-18	mg%	195.33	3.1	205.91	6.0	197.28	10.6	128.9	20.6	201.40	7.3	152.49	21.5	169.13	11.1	190.51	10.8	207.85	4.2	209.95	3.0	202.57	6.0	221.38	9.3	153.89	27.8	152.64	12.2	192.77	20.7	201.79	6.6	176.98	10.0	169.36	6.6	231.42	20.9			231.88	10.5	169.98	10.7			168.04	7.4	186.86	11.5	195.65	5.0	190.36	10.7	160.71	20.1	160.26	10.4			185.8	8.9					215.79	10.6	213.37	6.5	194.48	14.35			188.26	4.2			6/11/2003	MK Sullivan											12183685.01
Ethanol induced ataxia - acute functional tolerance (AFT) on dowel test [mg %]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		02	55-80 days	55	80	Male	6-18	mg%	65.2	4.3.	94.1	6.5	96.8	9.0	71.0	7.3	112.9	6.9	96.5	11.4	81.1	11.2	103.7	7.2	107.0	9.5	119.3	6.9	116.0	8.4	110.6	8.4	58.4	24.4	65.7	10.5	56.2	11.0	91.3	8.7	76.7	13.2	79.1	18.8	109.5	9.0			81.2	12.0	128.3	4.1			79.2	8.4	85.0	6.4	92.3	7.6	49.3	15.9	64.4	10.2	98.3	5.3			63.5	14.0					47.2	4.6	87.0	8.3	96.9	8.6			106.9	5.9			6/11/2003	MK Sullivan											12183685.02
Ethanol induced ataxia - time for loss of balance on dowel test [min]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		03	55-80 days	55	80	Male	6-18	minutes	2.09	0.17	2.33	2.33	1.75	0.14	1.03	.22	2.30	0.20	1.47	0.22	2.11	0.51	1.55	0.30	1.82	0.19	2.19	0.31	2.20	0.44	1.81	0.36	1.83	0.46	1.20	0.10	1.38	0.18	2.47	0.35	2.32	0.56	1.41	0.18	3.47	0.51			3.22	0.48	1.64	0.32			1.56	0.18	2.25	0.56	1.71	0.19	2.28	0.41	1.44	0.19	1.60	0.29			1.44	0.11					1.57	0.18	1.56	0.10	2.02	0.27			1.63	0.19			6/11/2003	MK Sullivan	ejc										12183685.03
Ethanol induced ataxia - time for regain of balance on dowel test (1) [min]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		04	55-80 days	55	80	Male	6-18	minutes	10.53	1.09	9.61	1.47	16.36	3.99	27.99	5.83	14.12	3.24	10.75	2.47	14.07	2.64	9.70	1.11	11.98	3.99	14.21	1.89	24.58	5.69	17.73	4.18	10.70	2.11	34.74	7.17	32.70	9.83	15.12	2.88	11.38	2.30	32.69	5.43	15.11	2.96			13.39	4.86	14.39	3.32			16.12	3.59	9.24	1.08	7.99	0.97	18.67	3.75	56.55	8.57	24.92	4.69			26.70	2.01					24.18	2.96	20.31	5.42	9.39	1.85			9.36	2.42			6/11/2003	MK Sullivan											12183685.04
Ethanol induced ataxia - time for regain of balance on dowel test (2) [min]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		05	55-80 days	55	80	Male	6-18	minutes	162.53	7.90	133.15	6.13	139.07	5.46	181.94	7.62	128.10	12.34	141.62	4.76	144.50	4.68	126.94	6.94	131.42	7.19	140.10	4.30	142	14.34	129.97	8.62	164.01	14.09	175.99	12.15	183.48	10.59	132.35	7.22	127.23	9.36	175.02	16.38	149.64	6.02			141.95	6.18	133.14	13.32			144.59	10.33	125.47	5.22	118.80	5.48	173.19	12.50	220.28	8.87	152.77	7.57			189.91	8.61					198.64	5.18	162.91	14.52	137.19	8.09			109.16	2.55			6/11/2003	MK Sullivan											12183685.05
Cerebellar cAMP accumulation - 1 micro-Molar basal		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		06	55-80 days	55	80	Male	6-18	micro-Molar	.608	0.076	1.48	0.191	1.23	0.074	1.1	.151	1.15	0.154	1.26	0.179	1.14	0.297	1.04	0.055	1.04	0.094	1.26	0.165	0.688	0.125	.994	0.074	1.87	0.141	1.15	0.147	0.972	0.228	1.38	0.166	.850	0.121	1.31	0.273	0.885	.0125			0.819	0.208	1.34	0.273			1.18	0.174	1.04	0.088	1.37	0.138	0.866	0.100	.866	0.215	1.43	0.152			1.11	0.199					.850	0.137	1.06	0.123	.868	0.114			1.21	0.172			6/11/2003	MK Sullivan											12183685.06
Cerebellar cAMP accumulation - 10 micro-Molar Forskolin		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		07	55-80 days	55	80	Male	6-18	micro-Molar	18.5	1.02	22.8	1.55	18.6	0.43	22.3	2.9	18.9	1.62	18.3	1.26	18.6	1.53	24.5	1.47	21.7	1.04	26.2	2.40	17.4	0.63	29.0	1.28	25.2	1.09	20.9	0.90	18.4	0.52	27.7	2.20	17.1	1.36	18.9	1.15	19.4	1.22			18.7	1.83	20.9	0.74			21.6	1.89	21.7	0.99	20.1	1.81	18.5	1.33	17.0	1.13	18.6	1.62			21.3	2.98					19.2	1.31	22.8	0.93	18.8	1.16			22.5	1.78			6/11/2003	MK Sullivan											12183685.07
Cerebellar cAMP accumulation - 1 micro-Molar isoproterenol		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		08	55-80 days	55	80	Male	6-18	micro-Molar	3.37	0.29	6.00	0.40	4.77	0.21	3.68	0.42	4.23	0.44	4.24	0.69	4.31	0.69	6.37	0.11	5.05	0.25	5.17	0.26	4.29	0.37	5.15	0.35	9.38	0.47	5.19	0.29	4.27	0.38	5.14	0.31	4.83	0.34	5.63	0.29	4.81	0.38			5.88	0.71	5.41	0.32			4.34	0.25	4.62	0.36	5.51	0.55	3.81	0.51	4.10	0.42	4.85	0.40			4.80	0.25					5.15	0.38	5.23	0.23	4.27	0.31			5.24	0.32			6/11/2003	MK Sullivan											12183685.08
Dopamine transporter expression DAT Bmax [pmol/mg]		Binding of 3beta-(4-iodophenyl) tropane-2beta-carboxylic acid methyl ester ([125I]RTI-55) to the dopamine transporter (DAT) in neostriatum from C57BL/6J, DBA/2J, and 21 BXD recombinant inbred (RI) mouse strains indicated highly significant strain differences in DAT density (Bmax) but no significant differences in affinity (Kd) for this radioligand. Strain mean Bmax values and the known genomic locations of 1390 marker loci were used to carry out a genome-wide search for quantitative trait loci (QTLs), which are chromosomal sites containing genes that influence DAT expression. This search revealed an unusually large effect QTL on chromosome 19 in the region of the proopiomelanocortin pseudogene Pomc-ps1 (8-11 cM), homologous to regions of human chromosomes 9q21 and 11q12-13. This QTL (logarithm of the odds 4.7, df = 1, p = 3 x 10(-6)) by conservative estimates accounts for just over half of the genetic variation in DAT binding site density. The QTL is not the DAT gene itself (Dat1, chromosome 13), but a powerful modulator of DAT expression in neostriatum. Furthermore, DAT expression levels in 20 of the BXD RI strains and the chromosome 19 QTL were correlated with cocaine and methamphetamine-induced locomotor activation and thermic responses (hypo- or hyperthermia), but were not correlated with behaviors related to sensitization, reward, voluntary consumption, stereotypy, or seizures induced by these two psychostimulant drugs. The results suggest that there is a gene(s) on proximal chromosome 19 that strongly influences DAT expression in neostriatum and may influence psychostimulant-induced activity and thermal responses.	Janowsky A, Mah C, Johnson RA, Cunningham CL, Phillips TJ, Crabbe JC, Eshleman AJ, Belknap JK.	Mapping genes that regulate density of dopamine transporters and correlated behaviors in recombinant inbred mice.	J Pharmacol Exp Ther	298(2)	634-643	Aug	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11454925&dopt=Abstract	11454925		01	50-60 days	50	60	Male	3-11	pmol/mg	2.28	0.2	3.37	0.7	2.15	0.3	1.96	0.2			3.95	1.2	5.26	0.6	3.22	0.5	3.86	0.6	2.52	0.8			1.68	0.4	3.33	1.4	5.29	1.1	2.32	0.2	1.65	0.1			3.22	0.5					4.85	0.6	2.91	0.5	4.20	0.4	2.45	0.3	3.11	0.3	3.38	0.2	2.83	0.2	1.93	0.2																							6/10/2003	MK Sullivan											11454925.01
Total hippocampus Volume - uncorrected for sex age body and brain weight		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		2003					.91	38-359 days	38	359	MF		mm3	28.0	0.7	24.3	0.5	28.4	0.8	22.4	0.5	26.7	0.9			28.0	1.2	22.5	0.5	25.7	1.1	25.3	0.7	23.7	0.7	24.6	0.7	27	0.7	22.7	0.6	24.5	0.5	27.4	0.9	21.7	0.7			26.8	0.4	23.6	0.8	23.6	0.5	22.5	1.1	20.4	0.8	21.3	0.6	20.4	0.8	18.9	0.7	23.7	0.7	26.6	0.9	21.6	0.6	20.5	0.7	23.0	0.5	23.6	0.7			24.1	0.5	22.2	0.7	27.4	1.0			25.4	0.6			7/25/2003	MK Sullivan											.0091
Hippocampus proper volume - uncorrected for sex age body and brain weight [mm3]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		2003					.92	38-359 days	38	359	MF		mm3	22.4	0.6	19.7	0.4	23.0	0.6	18.7	0.4	21.4	0.7			22.3	1.0	18.1	0.4	21.3	0.8	20.5	0.6	19.2	0.6	19.7	0.6	21.9	0.5	18.9	0.7	19.6	0.4	22.2	0.6	17.6	0.7			21.3	0.3	19.2	0.7	19.3	0.4	18.2	0.8	16.7	0.7	17.1	0.5	16.3	0.7	15.2	0.5	19.3	0.5	21.6	0.8	17.5	0.5	16.8	0.5	18.5	0.3	19.3	0.5			19.8	0.4	17.9	0.6	22.2	0.8			20.2	0.4			7/25/2003	MK Sullivan											.0092
Hippocampus pyramidal cell layer volume - uncorrected for sex age body and brain weight [mm3]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain BehavGenes Brain Behav	2	238-252		2003					.93	38-359 days	38	359	MF		mm3	1.41	0.11	1.18	0.06	1.68	0.09	1.42	0.04	1.60	0.12			1.69	0.10	1.38	0.04	1.60	0.11	1.58	0.09	1.46	0.07	1.61	0.14	1.58	0.09	1.37	0.03	1.55	0.07	1.74	0.15	1.16	0.08			1.49	0.07	1.44	0.11	1.47	0.10	1.43	0.08	1.336	0.11	1.33	0.12	1.15	0.06	1.24	0.07	1.43	0.11	1.48	0.06	1.39	0.08	1.38	0.06	1.38	0.04	1.46	0.06			1.64	0.11	1.23	0.07	1.65	0.14			1.48	0.07			7/25/2003	MK Sullivan											.0093
Hippocampus granule cell layer volume - uncorrected for sex age body and brain weight [mm3]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		2003					.94	38-359 days	38	359	MF		mm3	1.09	0.05	0.75	0.02	1.06	0.03	0.75	0.03	0.99	0.07			1.13	0.05	0.85	0.03	1.00	0.12	0.87	0.04	0.95	0.05	1.10	0.06	0.85	0.05	0.50	0.03	0.87	0.02	0.97	0.04	0.75	0.04			1.01	0.06	0.80	0.04	0.84	0.05	0.94	0.08	0.75	0.08	0.84	0.06	0.69	0.05	0.79	0.06	0.78	0.07	0.91	0.04	0.74	0.03	0.66	0.04	0.85	0.04	0.76	0.05			0.84	0.03	0.96	0.04	1.04	0.09			1.05	0.05			7/25/2003	MK Sullivan											.0094
Hippocampus dentate gyrus volume - uncorrected for sex age body and brain weight [mm3]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		2003					.95	38-359 days	38	359	MF		mm3	5.63	0.14	4.55	0.13	5.44	0.21	3.74	0.12	5.31	0.22			5.71	0.16	4.39	0.06	4.45	0.30	4.72	0.18	4.52	0.11	4.95	0.18	5.17	0.24	3.86	0.21	4.86	0.14	5.25	0.31	4.05	0.07			5.47	0.18	4.35	0.17	4.39	0.11	4.3	0.25	3.7	0.19	4.21	0.11	4.07	0.15	3.74	0.23	4.37	0.16	4.94	0.19	4.13	0.12	3.69	0.14	4.55	0.23	4.30	0.17			4.38	0.09	4.23	0.09	5.19	0.30			5.20	0.22			7/25/2003	MK Sullivan											.0095
Body Weight [g]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		20032003					.96	38-359 days	38	359	MF		g	28.6	2.2	25.9	1.3	20.7	1.2	21.9	1.5	28.3	0.6			24.3	1.5	23.9	1.8	19.1	1.9	23.2	1.4	23.1	1.3	23.2	1.4	28.7	0.7	23.5	1.3	22.0	1.9	21.2	1.4	21.7	1.6			25.5	2.4	18.3	1.4	25.8	1.9	15.7	1.3	23.5	2.3	21.3	1.3	16.9	1.5	18.2	1.5	22.0	3.2	25.3	1.8	20.5	1.1	23.5	0.5	19.9	0.9	19.7	2.2			20.2	1.4	18.5	1.1	18.5	1.3			21.2	0.8			7/25/2003	MK Sullivan											.0096
Brain Weight [mg]		We recently mapped two quantitative trait loci that have widespread effects on hippocampal architecture in mouse: Hipp1a and Hipp5a. We also noted remarkable strain differences in the relative sizes of different hippocampal regions. Estimated heritable variation for these differences was 42% in hippocampus proper, 40% in dentate gyrus, 31% in granule cell layer and 18% in pyramidal cell layer. Region size varied at least 50% from largest to smallest measurement. Here we have utilized these differences to identify loci with effects on the dentate gyrus, granule cell layer, hippocampus proper, and pyramidal cell layer. Our sample consists of C57BL/6J and DBA/2J and 32 BXD recombinant inbred strains. Volumetric data were corrected for shrinkage and for differences in brain weight. We identified significant loci on chromosomes (Chr) 6, 13 and 15, and significant interaction locus on proximal Chr 11. A suggestive distal Chr 1 locus overlaps with Hipp1a. HipV13a (Chr 13, 42-78 Mb) has an additive effect of 0.56 mm3 (12.1%) on dentate gyrus volume, while GrV6a (Chr 6, 29-65 Mb) has additive effects of 0.14 mm3 (16.0%) on the volume of the granule cell layer. HipV13a also interacts with DGVi11a, a locus on proximal Chr 11 that operates exclusively through its epistatic effect on HipV13a and has no independent main effect. HipV15a (Chr 15, 0-51 Mb) has an additive effect of 1.76 mm3 (9.0%) on the volume of the hippocampus proper. We used WebQTL, a recently described web-based tool, to examine genetic correlation of gene expresssion with hippocampal volume. We identified a number of genes that map within the QTL intervals and have highly correlated expression patterns. Using WebQTL's extensive database of published BXD phenotypes, we also detected a strong and potentially biologically meaningful correlation between hippocampal volume and acoustic startle response.	Peirce JL, Chesler EJ, Williams RW, Lu L	Genetic architecture of the mouse hippocampus:  Identification of gene loci with selective regional effects	Genes Brain Behav	2	238-252		2003					.97	38-359 days	38	359	MF		mg	477.4	4.8	401.4	5.6	458.0	7.3	426.6	5.9	544.9	9.4			424.8	10.4	434.9	2.7	429.0	9.7	438.4	8.5	417.7	4.0	44.4	8.6	453.1	4.4	435.6	11.6	418.0	5.0	425.4	6.7	392.2	3.2			458.2	6..5	414.1	5.2	408.1	3.9	391.9	9.8	358.0	4.9	395.4	4.7	371.7	9.2	361.2	11.4	402.2	11.4	446.0	6.6	429.2	6.4	413.5	5.7	410.0	5.8	409.3	7.4			415.6	5.9	396.6	7.8	429.7	4.7			454.5	5.4			7/25/2003	MK Sullivan											.0097
Relative frequency of audiogenic seizure [%]		Mice of some inbred strains, such as 21-day-old DBA/2J mice, have generalized convulsions when exposed to intense auditory stimulation. Analysis of susceptibility to audiogenic seizures in BXD recombinant inbred strains has demonstrated the influence of at least three loci. One locus, Asp-1, is located on chromosome 12 between Ah and D12Nyu1; another locus, Asp-2, is on chromosome 4, tightly linked to b. Here we report evidence that Asp-2 is located within an 8-centimorgan segment distal to b and that Asp-3 is linked to Mtv-1 on chromosome 7. We also present evidence that these three loci account for most of the heritable variation in susceptibility to audiogenic seizures in crosses of DBA/2J and C57BL/6J mice and that susceptibility to audiogenic seizures is influenced by genomic imprinting. Thus, genomic imprinting may complicate linkage and mapping studies and should be considered in analyses of complex modes of inheritance.	Neumann PE, Collins RL	Genetic dissection of susceptibility to audiogenic seizures in inbred mice.	Proc Natl Acad Sci	88(12)	5408-5412	Jun 	1991 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2052619&dopt=Abstract	2052619		01	21 days	21		MF		%	2		91		0		92		68		0		23		93		21		0		0		8		94		0		0		35				92				40		22		0		29		22		0		0				90																								7/1/2003	MK Sullivan	MK Sullivan										2052619.01
Ethanol metabolism-2 g/kg [mg/ml/hr]		BACKGROUND: Genetic factors are well known to play an important role in determining individual differences in the metabolism of ethanol (EtOH), and several specific polymorphic loci have been identified that significantly contribute to the variability of EtOH metabolism in humans. However, these variant genes are either alcohol or aldehyde dehydrogenases, and the identification of new gene products that contribute to variation in alcohol metabolism would be useful. METHODS: To identify quantitative trait loci (QTLs), we correlated variation in polymorphic markers with blood EtOH concentration and the rate of EtOH metabolism (beta) in C57BL/6J and DBA/2J strains and in 25 of their recombinant inbred strains after 2 and 3 g/kg of EtOH intraperitoneally. RESULTS: A QTL associated with beta values for both doses was definitively mapped to the proximal region of chromosome 17, syntenic with human chromosome 6q25-27. Seven to 12 chromosomal regions were provisionally identified for each phenotype; several were associated with 2 or more phenotypes. Each QTL suggests the location of a gene or genes affecting EtOH pharmacokinetics. Candidate genes suggested by these analyses included several whose gene products are known to be induced by EtOH (e.g., superoxide dismutase, glutathione transferase, and cytochrome P450 2E1), as well as several whose gene products have signaling functions likely to contribute to this induction. CONCLUSIONS: These studies provide evidence for the existence of genes affecting EtOH metabolism in multiple chromosomal regions. Future studies will be required to identify the chromosome 17 gene product. Use of other genetic populations, such as B6D2F2 crosses, will be required to determine which of the provisional loci represent true and which represent false-positive associations.	Grisel JE, Metten P,                                                                                                                                                                                                                                                                                        Wenger CD, Merrill CM, Crabbe JC	Mapping of quantitative trait loci underlying ethanol metabolism in BXD recombinant inbred mouse strains.	Alcohol Clin Exp Res 	26(5)	610-616	May	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12045468&dopt=Abstract	12045468		01	7-16 wks	49	112	Male	10-28	mg/ml/hr	-0.72	0.02	-0.92	0.01	-0.79	0.02	-0.8	0.02	-0.68	0.10	-0.64	0.02	-0.82	0.07	-0.80	0.02	-0.87	0.04	-0.64	0.01	-0.83	0.01	-0.95	0.04	-0.97	0.01	-0.76	0.04	-0.73	0.04	-0.82	0.04			-0.84	0.04	-0.84	0.01	-0.97	0.04	-0.92	0.02	-0.77	0.01	-0.96	0.01	-0.77	0.02	-1.00	0.02	-0.63	0.04	-0.68	0.04	-0.73	0.05																							6/5/2003	MK Sullivan											12045468.01
Ethanol metabolism-3 g/kg [mg/ml/hr]		BACKGROUND: Genetic factors are well known to play an important role in determining individual differences in the metabolism of ethanol (EtOH), and several specific polymorphic loci have been identified that significantly contribute to the variability of EtOH metabolism in humans. However, these variant genes are either alcohol or aldehyde dehydrogenases, and the identification of new gene products that contribute to variation in alcohol metabolism would be useful. METHODS: To identify quantitative trait loci (QTLs), we correlated variation in polymorphic markers with blood EtOH concentration and the rate of EtOH metabolism (beta) in C57BL/6J and DBA/2J strains and in 25 of their recombinant inbred strains after 2 and 3 g/kg of EtOH intraperitoneally. RESULTS: A QTL associated with beta values for both doses was definitively mapped to the proximal region of chromosome 17, syntenic with human chromosome 6q25-27. Seven to 12 chromosomal regions were provisionally identified for each phenotype; several were associated with 2 or more phenotypes. Each QTL suggests the location of a gene or genes affecting EtOH pharmacokinetics. Candidate genes suggested by these analyses included several whose gene products are known to be induced by EtOH (e.g., superoxide dismutase, glutathione transferase, and cytochrome P450 2E1), as well as several whose gene products have signaling functions likely to contribute to this induction. CONCLUSIONS: These studies provide evidence for the existence of genes affecting EtOH metabolism in multiple chromosomal regions. Future studies will be required to identify the chromosome 17 gene product. Use of other genetic populations, such as B6D2F2 crosses, will be required to determine which of the provisional loci represent true and which represent false-positive associations.	Grisel JE, Metten P, Wenger CD, Merrill CM, Crabbe JC	Mapping of quantitative trait loci underlying ethanol metabolism in BXD recombinant inbred mouse strains.	Alcohol Clin Exp Res 	26(5)	610-616	May	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12045468&dopt=Abstract	12045468		02	7-16 wks	49	112	Male	10-28	mg/ml/hr	-0.69	0.02	-0.83	0.00	-0.71	0.02	-0.72	0.05	-0.71	0.02	-0.69	0.01	-0.88	0.02	-0.85	0.04	-0.8	0.03	-0.51	0.02	-0.74	0.04	-0.85	0.01	-0.83	0.02	-0.67	0.04	-0.72	0.02	-0.73	0.04			-0.85	0.02	-0.75	0.04	-0.88	0.04	-0.86	0.02	-0.74	0.04	-0.92	0.03	-0.76	0.02	-0.83	0.01	-0.59	0.02	-0.62	0.01	-0.65	0.02																							6/5/2003	MK Sullivan											12045468.02
Blood Ethanol Concentration 60 minutes after 2 g/kg [mg/ml]		BACKGROUND: Genetic factors are well known to play an important role in determining individual differences in the metabolism of ethanol (EtOH), and several specific polymorphic loci have been identified that significantly contribute to the variability of EtOH metabolism in humans. However, these variant genes are either alcohol or aldehyde dehydrogenases, and the identification of new gene products that contribute to variation in alcohol metabolism would be useful. METHODS: To identify quantitative trait loci (QTLs), we correlated variation in polymorphic markers with blood EtOH concentration and the rate of EtOH metabolism (beta) in C57BL/6J and DBA/2J strains and in 25 of their recombinant inbred strains after 2 and 3 g/kg of EtOH intraperitoneally. RESULTS: A QTL associated with beta values for both doses was definitively mapped to the proximal region of chromosome 17, syntenic with human chromosome 6q25-27. Seven to 12 chromosomal regions were provisionally identified for each phenotype; several were associated with 2 or more phenotypes. Each QTL suggests the location of a gene or genes affecting EtOH pharmacokinetics. Candidate genes suggested by these analyses included several whose gene products are known to be induced by EtOH (e.g., superoxide dismutase, glutathione transferase, and cytochrome P450 2E1), as well as several whose gene products have signaling functions likely to contribute to this induction. CONCLUSIONS: These studies provide evidence for the existence of genes affecting EtOH metabolism in multiple chromosomal regions. Future studies will be required to identify the chromosome 17 gene product. Use of other genetic populations, such as B6D2F2 crosses, will be required to determine which of the provisional loci represent true and which represent false-positive associations.	Grisel JE, Metten P, Wenger CD, Merrill CM, Crabbe JC	Mapping of quantitative trait loci underlying ethanol metabolism in BXD recombinant inbred mouse strains.	Alcohol Clin Exp Res 	26(5)	610-616	May	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12045468&dopt=Abstract	12045468		03	7-16 wks	49	112	Male	10-28	mg/ml	1.930	0.043	2.249	0.083	1.859	0.059	1.861	0.054	1.848	0.040	1.654	0.050	2.113	0.097	2.228	0.086	1.907	0.093	1.447	0.019	2.002	0.072	2.010	0.063	1.927	0.076	2.089	0.085	1.767	0.070	1.749	0.077			1.833	0.046	1.861	0.062	1.969	0.048	2.337	0.065	1.794	0.053	1.996	0.117	1.935	0.049	1.864	0.063	1.627	0.065	1.560	0.050	1.615	0.059																							6/5/2003	MK Sullivan											12045468.03
Blood Ethanol Concentration 60 minutes after 3 g/kg  [mg/ml]		BACKGROUND: Genetic factors are well known to play an important role in determining individual differences in the metabolism of ethanol (EtOH), and several specific polymorphic loci have been identified that significantly contribute to the variability of EtOH metabolism in humans. However, these variant genes are either alcohol or aldehyde dehydrogenases, and the identification of new gene products that contribute to variation in alcohol metabolism would be useful. METHODS: To identify quantitative trait loci (QTLs), we correlated variation in polymorphic markers with blood EtOH concentration and the rate of EtOH metabolism (beta) in C57BL/6J and DBA/2J strains and in 25 of their recombinant inbred strains after 2 and 3 g/kg of EtOH intraperitoneally. RESULTS: A QTL associated with beta values for both doses was definitively mapped to the proximal region of chromosome 17, syntenic with human chromosome 6q25-27. Seven to 12 chromosomal regions were provisionally identified for each phenotype; several were associated with 2 or more phenotypes. Each QTL suggests the location of a gene or genes affecting EtOH pharmacokinetics. Candidate genes suggested by these analyses included several whose gene products are known to be induced by EtOH (e.g., superoxide dismutase, glutathione transferase, and cytochrome P450 2E1), as well as several whose gene products have signaling functions likely to contribute to this induction. CONCLUSIONS: These studies provide evidence for the existence of genes affecting EtOH metabolism in multiple chromosomal regions. Future studies will be required to identify the chromosome 17 gene product. Use of other genetic populations, such as B6D2F2 crosses, will be required to determine which of the provisional loci represent true and which represent false-positive associations.	Grisel JE, Metten P, Wenger CD, Merrill CM, Crabbe JC	Mapping of quantitative trait loci underlying ethanol metabolism in BXD recombinant inbred mouse strains.	Alcohol Clin Exp Res 	26(5)	610-616	May	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12045468&dopt=Abstract	12045468		04	7-16 wks	49	112	Male	10-28	mg/ml	3.145	0.094	3.464	0.108	2.434	0.123	2.847	0.110	2.951	0.089	2.895	0.092	3.284	0.057	3.562	0.120	2.894	0.119	2.606	0.058	3.570	0.071	3.076	0.078	2.951	0.042	3.326	0.071	2.903	0.063	3.185	0.134			3.084	0.045	2.702	0.076	2.975	0.068	3.652	0.110	3.826	0.135	3.544	0.123	3.198	0.071	2.956	0.063	2.828	0.084	2.395	0.115	2.325	0.077																							6/5/2003	MK Sullivan											12045468.04
Total Hippocampus granule cell number [number of cells]		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH.	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		01				MF	1-10	number of cells	344252	17444	298849	12466			281933	37464	386307	9386	435866	67540	343767	29226					303769										308851	2741	335002	2965											292057	13429			309037	16105	348995	18523	284144	12553																											6/14/2003	MK Sullivan									table 2		12153537.01
Age Related T-Cell Decline - Concavalin-A induced Thymic T-Cell proliferative response (average of days 2 and 4) 		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		01	22 months	~671		Female	2-4		9933	3647	5404	1259											2782		218		0						9115	1725			6777	684	911	389					1298	478	175	92	5033		8719	954	11363	1045	47862	5486	24487	8662					135191																								7/29/2003	MK Sullivan											12044964.01
Metastasis of Implanted Breast Tumor - Lymph node (note: proportion of 5 mice) [number of mice with tumor metastasis] 		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		01	12 months	365		Female	5	number of mice with tumor metastasis 	0		0		0				0						0		0		0								0								0						5		3		0		4				5		3		0																								7/3/2003	MK Sullivan											12209979.01
Metastasis of Implanted Breast Tumor - Pancreas (note: proportion of 5 mice) [number of mice with tumor metastasis]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		02	12 months	365		Female	5	number of mice with tumor metastasis 	0		0		0				0						0		0		0								0								0						3		2		0		3				2		3		0																								7/3/2003	MK Sullivan											12209979.02
Necrosis of Implanted Breast Tumor (note: proportion of 5 mice) [number of mice with tumor metastasis]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		03	12 months	365		Female	5	number of mice with tumor metastasis 	0		1		0				0						0		0		0								0								0						5		5		0		5				5		5		0																								7/3/2003	MK Sullivan											12209979.03
Age Related Thymic involution slope (-Beta1x10^4)			Hsu H-C, Zhang H-G, Li L, Yi N, Yang P-A, Wu Q, Wu Y, Renda J, Xu X, Yang X-W, Lu L,  Van Zant G, Williams RW, Allison DB, Mountz JD.	Age-related thymic involution in C57BL/6J x DBA/2J recombinant inbred mice maps to chromosomes 9 and 10.										70				Female			41	3	49	4	37	3					35	9	132	5	30	9	45	9	50	2			59 	4	37	9	52	3	62	7	26	3					52	10			65	11			36	17	52	9	34	7			66	4	56	8																					39	3													.7
Age Related T-Cell Decline % of CD4 negative CD8 negative DN cells [%]		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		02	22 months	~671		Female	2-4	%	3.8	0.4	11.4	0.7											3.7		16		44.4	12.5					8.7	1.5			5.8	1.1	11.5	2.4					8.8	0.8	5.9	1.2	33.5		5.4	0.6	5.3	0.7	8	1.5	6.1	2.3					2.2																								7/29/2003	MK Sullivan											12044964.02
Age Related T-Cell Decline % of CD4 positive CD8 positive DP cells [%]		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		03	22 months	~671		Female	2-4	%	84.6	1.3	68.4	4.1											86.9		64.2		43.7	13.4					80.5	6.9			64.7	3.8	70.1	6.7					73	4.6	76.4	15.2	43.6		87.3	2.8	82.1	5.5	77.1	4.5	81.5	4.2					90.1																								7/29/2003	MK Sullivan											12044964.03
Age Related T-Cell Decline % of CD25 negative CD44 positive DN cells [%]		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		04	22 months	~671		Female	2-4	%	41.2	3.2	20	5.6											21.5		45.2		55.5	15.3					40.0	3.6			22	8.5	37.3	10.1					41.8	1.6	17.1	1.2	15		16.8	4.1	32.4	4.9	43.9	3.5	39.4	4.3					20.5																								7/29/2003	MK Sullivan											12044964.04
Age Related T-Cell Decline % of CD25 positive CD44 negative DN cells [%]		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		05	22 months	~671		Female	2-4	%	13.2	1.5	2.1	0.7											32.9		12		2.4	0.8					28.2	1.2			6.3	0.5	20.4	3.2					19.8	4.5	25.8	5.1	1.5		12.9	2.3	18.6	4.9	16.6	5.8	15.3	7.6					22.8																								7/29/2003	MK Sullivan											12044964.05
Age Related T-Cell Decline % of CD25 negative CD44 negative DN cells [%]		Age-related decline in thymic T-cell development in 22-month-old C57BL/6J X DBA/2J (BXD) recombinant inbred strains of mice was functionally and phenotypically analyzed and genetically mapped. There was a positive correlation of the concanavalin A (Con A)-induced thymocyte proliferative response with the capability of thymocytes to mature to the CD4(+)CD8(+) stage. The accumulation of CD4(-)CD8(-) stage of thymocytes in 22-month-old BXD mice was further identified to be associated with a developmental block between the CD25(-)CD44(+) and the CD25(+)CD44(+) stages. The quantitative trait loci regulating the Con A-induced thymocyte proliferative response were mapped to mouse chromosome 1, 3, and 11, nearest to 32.1 centimorgan (cM), 5.6 cM, and 18.0 cM, respectively. Our results suggest that several genetic loci regulate the intra-thymic T-cell maturation process and play an important role in determining age-related decline in thymic T-cell development.	Hsu HC, Mountz JD, Williams RW, Shelton BJ, Yang PA, Matsuki Y, Xu X, Dodd CH, Li L, Geiger H, Zhang HG, Van Zant G	Age-related change in thymic T-cell development is associated with genetic loci on mouse chromosomes 1, 3, and 11	Mech Ageing Dev 	123(8)	1145-1158	Apr	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12044964&dopt=Abstract	12044964		06	22 months	~671		Female	2-4	%	43.6	2.5	78.2	6.4											44.5		40.5		42.7	12.7					28.9	3.8			71.9	15.3	37.6	8.5					36.8	1.8	66.7	14.2	82.3		71.8	6.1	46	3.4	36.6	6.3	44.2	11.2					56.4																								7/29/2003	MK Sullivan											12044964.06
Implanted Breast Tumor Growth - Tumor Type (note: ordered categorical data) [number of mice with tumor metastasis] 		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		04	12 months	365		Female	5	number of mice with tumor metastasis 	4		2		4				4						3		2		3								2								4						1		1		3		1				1		1		2																								7/3/2003	MK Sullivan											12209979.04
Thymocyte Count initial (Beta 0)			Hsu H-C, Zhang H-G, Li L, Yi N, Yang P-A, Wu Q, Wu Y, Renda J, Xu X, Yang X-W, Lu L,  Van Zant G, Williams RW, Allison DB, Mountz JD.	Age-related thymic involution in C57BL/6J x DBA/2J recombinant inbred mice maps to chromosomes 9 and 10.										71				Female			23.3	2	10.4	1.6	28.4	3.3					26.5	3.9	32.6	8.3	17.3	4.9	24.6	5.7	15.2	4.2			37.2	4	36.4	4.2	21.5	3.6	26.7	13.4	22	4.2					33.2	4.9			30	11			39.7	4.3	16.4	3.9	35.2	6.5			33.3	6.9	14.1	4.1																					25.5	9.6													.71
Projected day 60 Thymocyte count			Hsu H-C, Zhang H-G, Li L, Yi N, Yang P-A, Wu Q, Wu Y, Renda J, Xu X, Yang X-W, Lu L,  Van Zant G, Williams RW, Allison DB, Mountz JD.	Age-related thymic involution in C57BL/6J x DBA/2J recombinant inbred mice maps to chromosomes 9 and 10.										72				Female			23.1		10.8		29.2						24.9		39.1		16.4		25.1		20.4				37.3		37.5		25		27.9		22.2						29.8				32.6				40.8		18.9		40.4				34.9		16.7																						24.9														.72
Morris Water Maze - Log Latency 1		The Morris navigation task is widely used to study spatial abilities in rodents; namely, to analyze the effects of mutations in genetically engineered mice. Although quantitative and Mendelian genetic studies have shown that the variation of these abilities is partly under genetic control, little is known about these genetic factors. In order to analyze the genetic architecture of spatial navigation in mice, a wide genome scan was performed to map the QTLs that control various aspects of the performance, using the RI strain methodology. Latencies to locate the submerged platform across learning sessions and performance to the spatial probe test were analyzed in the 26 strains of the B x D RI series. Both cluster analysis of behavioral measurements and QTL mapping confirmed previous data showing that the escape latencies and the spatial bias rely on two distinct components of the task, controlled by different loci. A QTL on chromosome 1 influenced escape latencies during the four training sessions, whereas another QTL, located on chromosome 5, was shown to control spatial performance at the probe trial and also exhibited epistatic interactions with two other QTLs on chromosomes 2 and 13. The function of these QTLs is examined in the broader context of hippocampal-dependent learning processes and in relation to QTLs already found in similar positions in other behavioral traits.	Milhaud JM, Halley H, Lassalle JM.	Two QTLs located on chromosomes 1 and 5 modulate different aspects of the performance of mice of the B x D Ty RI strain series in the Morris navigation task	Behav Genet	32(1)	69-78	Jan	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11958544&dopt=Abstract	11958544		01											1.814		1.432		1.254		1.646		1.463		1.277		1.357		1.674		1.636		1.43		1.854		1.571		1.64		1.578		1.746		1.803		1.352		1.365		1.51		1.346		1.657		1.67		1.795		1.59		1.597		1.371																																				11958544.01
Morris Water Maze - Log Latency 2		The Morris navigation task is widely used to study spatial abilities in rodents; namely, to analyze the effects of mutations in genetically engineered mice. Although quantitative and Mendelian genetic studies have shown that the variation of these abilities is partly under genetic control, little is known about these genetic factors. In order to analyze the genetic architecture of spatial navigation in mice, a wide genome scan was performed to map the QTLs that control various aspects of the performance, using the RI strain methodology. Latencies to locate the submerged platform across learning sessions and performance to the spatial probe test were analyzed in the 26 strains of the B x D RI series. Both cluster analysis of behavioral measurements and QTL mapping confirmed previous data showing that the escape latencies and the spatial bias rely on two distinct components of the task, controlled by different loci. A QTL on chromosome 1 influenced escape latencies during the four training sessions, whereas another QTL, located on chromosome 5, was shown to control spatial performance at the probe trial and also exhibited epistatic interactions with two other QTLs on chromosomes 2 and 13. The function of these QTLs is examined in the broader context of hippocampal-dependent learning processes and in relation to QTLs already found in similar positions in other behavioral traits.	Milhaud JM, Halley H, Lassalle JM.	Two QTLs located on chromosomes 1 and 5 modulate different aspects of the performance of mice of the B x D Ty RI strain series in the Morris navigation task	Behav Genet	32(1)	69-78	Jan	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11958544&dopt=Abstract	11958544		02											1.483		1.244		1.094		1.405		1.444		1.257		1.176		1.427		1.505		1.395		1.603		1.414		1.463		1.565		1.51		1.551		1.176		1.341		1.204		1.169		1.337		1.392		1.587		1.26		1.513		1.219																																				11958544.02
Morris Water Maze - Log Latency 3		The Morris navigation task is widely used to study spatial abilities in rodents; namely, to analyze the effects of mutations in genetically engineered mice. Although quantitative and Mendelian genetic studies have shown that the variation of these abilities is partly under genetic control, little is known about these genetic factors. In order to analyze the genetic architecture of spatial navigation in mice, a wide genome scan was performed to map the QTLs that control various aspects of the performance, using the RI strain methodology. Latencies to locate the submerged platform across learning sessions and performance to the spatial probe test were analyzed in the 26 strains of the B x D RI series. Both cluster analysis of behavioral measurements and QTL mapping confirmed previous data showing that the escape latencies and the spatial bias rely on two distinct components of the task, controlled by different loci. A QTL on chromosome 1 influenced escape latencies during the four training sessions, whereas another QTL, located on chromosome 5, was shown to control spatial performance at the probe trial and also exhibited epistatic interactions with two other QTLs on chromosomes 2 and 13. The function of these QTLs is examined in the broader context of hippocampal-dependent learning processes and in relation to QTLs already found in similar positions in other behavioral traits.	Milhaud JM, Halley H, Lassalle JM.	Two QTLs located on chromosomes 1 and 5 modulate different aspects of the performance of mice of the B x D Ty RI strain series in the Morris navigation task	Behav Genet	32(1)	69-78	Jan	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11958544&dopt=Abstract	11958544		03											1.424		1.195		1.051		1.134		1.282		1.002		1.037		1.249		1.33		1.141		1.422		1.344		1.336		1.401		1.298		1.325		1.079		1.314		1.397		1.041		1.137		1.264		1.393		1.202		1.505		1.009																																				11958544.03
Brain weight [mg]		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									73							478	6.0	393	9.0	441	12.4	424	7.4	540	10.4			428	12.7	431	3.6	434	5.5	438	13.2	415	5.6	444	11.2	453	5.2	431	11.8	419	11.2	432	13.0	392	3.9			446	5.7	414	9.7	407	9.0	401	18.0	352	2.2	394	7.0	376	10.5	369	11.7	414	9.5	443	5.8	424	12.8	414	10.0	402	6.0	403	11.8			418	9.8	393	14.9	431	7.9			449	8.0															.73
Lateral Geniculate Nucleus Volume (mm3)		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									74							0.30	0.02	0.26	0.01	0.30	0.03	0.25	0.02	0.36	0.02			0.23	0.01	0.29	0.03	0.32	0.02	0.23	0.01	0.26	0.02	0.26	0.01	0.29	0.01	0.26	0.02	0.25	0.03	0.31	0.01	0.25	0.01			0.33	0.04	0.35	0.01	0.25	0.01	0.26	0.02	0.25	0.01	0.23	0.01	0.24	0.02	0.23	0.01	0.28	0.02	0.27	0.01	0.25	0.02	0.28	0.03	0.28	0.01	0.27	0.02			0.27	0.01	0.32	0.02	0.35	0.01			0.31	0.01															.74
Total Lateral Geniculate Nucleus Cell Number x 1000		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									75							46.7	2.0	37.0	1.7	36.9	2.5	34.6	2.0	46.4	2.1			34.8	2.1	41.7	3.5	41.9	3.8	36.3	1.9	39.7	5.2	37.3	1.4	41.4	1.4	48.2	2.3	38.7	4.6	35.7	4.1	41.0	3.1			0.33	0.04	0.35	0.01	38.6	0.9	35.0	3.6	31.5	1.6	36.3	2.9	37.2	2.7	36.5	1.5	43.8	1.5	34.2	1.1	38.4	2.7	40.6	1.7	39.3	2.7	40.0	2.6			36.0	1.1	39.3	2.9	43.0	1.9			39.8	3.0															.75
Total Lateral Geniculate Nucleus Neuron Number x 1000		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									76																																																																																																	.76
Total Lateral Geniculate Nucleus Glial Cell Number		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									77																																																																																																	.77
Total Lateral Geniculate Nucleus Endothelial Cell Number x 1000		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									78																																																																																																	.78
Total Retinal Ganglion Cell Number x 1000		The proliferation and survival of different cell types is thought to be modulatedduring development to achieve near optimal ratios and functional balance. Wehave tested the precision of coregulation of numbers of neurons, glial cells, andendothelial cells in the dorsal lateral geniculate nucleus (LGN) of 58 isogenicstrains of mice. We also acquired matched counts of retinal ganglion cells. Ouraim has been to test the precision of numerical matching among multiple celltypes in the primary visual system and to test the neurotrophic hypothesis. Allcells were counted using unbiased counting protocols and tissue that is part of theMouse Brain Library (www.mbl.org). Classification criteria were assessed in aparallel immunohistochemical analysis. The LGN contains an average of 17,000neurons, 12,000 glial cells, and 10,000 endothelial cells. There is substantialvariation around these meansÑgenerally, two-fold differences per cell type. Straindifferences in LGN volume correlate moderately well with glial cell number (r =0.61, p < 0.01), less so with retinal ganglion cell number (r = 0.41, p < 0.01), andsurprisingly weakly with the total population of neurons (r = 0.22, p < 0.10).Numbers of neurons and glial cells correlate only modestly (r = 0.40, p < 0.01).The single most surprising and unequivocal finding was the lack of any detectablecorrelation between populations of LGN neurons and retinal ganglion cellsÑacorrelation of merely 0.05 with a set of 57 strains. We conclude that numbers ofthese two functionally coupled cell populations are modulated over a wide rangeby independent genetic and developmental mechanisms.	Seecharan DJ, Kulkarni AL, Lu L, Rosen GD, Williams RW	Genetic Control of Interconnected Neuronal Populations in the Mouse Primary Visual System	submitted									79																																																																																																	.79
Drd1 expression in Nucleus Accumbens - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		01											1146.09		1218.17		1551.25		1431.13		1660.89		1385.05		724.54		1428.62		1437.34						807										1334.39				1747.8		858.06		1234.18				788.02				1345.13		1258.18																													MND1NA							10591541.01
Drd1 expression in Nucleus Accumbens - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		02											1165.17		898.7		1236.23		1319.21		1548.25		1407.51		693.2		1662.47		1112.43						1069.25										1415.07				1527.46		850.74		1108.99				559.63				1133.14		944.71																													M1D1NA							10591541.02
Drd1 expression in Nucleus Accumbens - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		03											1127		1537.64		1866.27		1543.04		1773.52		1362.6		755.89		1194.78		1762.26						544.75										1253.71				1968.13		865.37		1359.38				1016.41				1557.12		1571.65																													M2D1NA							10591541.03
Drd1 expression in Caudate Putamen - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		04											1042.12		1502.01		1181.74		1238.93		2496.82		1913.99		637.83		2071.32		2041.24						1124.94										2497.22				844.1		1433.32		1718.09				947.62				2229.84		1091.13																													M1D1CP							10591541.04
Drd1 expression in Caudate Putamen - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		05											678.67		1267.17		500.06		1001.61		2038.68		1812.29		892.36		1420.57		2169.59						579.79										1941.54				1983.04		1704.15		1780.39				1282.96				2015.38		1582.85																													M2D1CP							10591541.05
Drd1 expression in Caudate Putamen -  male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		06											860.395		1384.59		840.9		1120.27		2267.75		1863.14		765.095		1745.945		2105.415						852.365										2219.38				1413.57		1568.735		1749.24				1115.29				2122.61		1336.99																													MND1CP							10591541.06
Drd1 expression in Frontal Cortex - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		07											356		500.52		417.91		652.6		484.91		745.82		368.18		427.94		499.4						327.51										614.29				633.2		390.88		347.02				330.04				501.81		321.84																													M1D1FC							10591541.07
Drd1 expression in Frontal Cortex - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		08											222.5		673.62		1786.29		305.52		472.75		588.41		482.63		487.41		751.59						112.91										520.06				548.29		347.19		463.85				228.38				757.84		383.92																													M2D1FC							10591541.08
Drd1 expresion in Frontal Cortex - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		09											289.25		587.07		1102.1		479.06		478.83		667.115		425.405		457.675		625.495						220.21										567.175				590.745		369.035		405.435				279.21				629.825		352.88																													MND1FC							10591541.09
Drd1 expression in ventral midbrain - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		10											112.98		182.53		143.66		302.51		249.05		403.05		317.52		319.56		330.16						190.04										301.39				354.6		218.67		184.15				229.03				221.24		167.52																													M1D1VM							10591541.1
Drd1 expression in ventral midbrain - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		11											227.5		345.06		271.11		180.47		255.11		404.21		325.62		312.17		515.21						250.44										358.99				128.85		144.63		128.43				128.72				267.44		215.57																													M2D1VM							10591541.11
Drd1 expression in ventral midbrain - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		12											170.24		263.795		207.385		241.49		252.08		403.63		321.57		315.865		422.685						220.24										330.19				241.725		181.65		156.29				178.875				244.34		191.545																													MND1VM							10591541.12
Drd2 expression in Nucleus Accumbens - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		13											115.64		231.23		224.3		87.03		215.2		228.65		111.9		203.2		254.42						136.06										227.81				195.84		141.91	 	252.69		161.82		82.15				244.89		151.57																													M1D2NA							10591541.13
Drd2 expression in Nucleus Accumbens -  females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		14													308.7		321.67		101.75		200.61		212.38		81.26		222.68		210.88						130.91										171.23				151.59				159.22		186.64		72.13				228.88		175.66																													M2D2NA							10591541.14
Drd2 expression in Nucleus Accumbens - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct             	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		15											115.64		269.965		272.985		94.39		207.905		220.515		96.58		212.94		232.65						133.485										199.52				173.715		141.91		205.955		174.23		77.14				236.885		163.615																													MND2NA							10591541.15
Drd2 expression in Caudate Putamen - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		16											67.47		286.9		256.8		128.17		353.21		343.32		129.5		263.71		268.08						97.49										331.8				58.35		49.42		340.32		390.09		132.43				322.32		136.6																													M1D2CP							10591541.16
Drd2 expression in Caudate Putamen - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		17													362.04		68.75		146.81		378.43		270.03		92.48		167		245.4						129.03										320.61				175.18				288.78		298		163.73				400.11		271.82																													M2D2CP							10591541.17
Drd2 expression in Caudate Putamen - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		18											67.47		324.47		162.775		137.49		365.82		306.675		110.99		215.355		256.74						113.26										326.205				116.765		49.42		314.55		344.045		148.08				361.215		204.21																													MND2CP							10591541.18
Drd2 expression in Frontal Cortex -  males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		19											50.59		36.56		38.41		59.81		50.9		64.47		44.77		47.49		62.96						28.51										57.87				42.6		25.91		63.01		66.75		44.71				83.44		23.54																													M1D2FC							10591541.19
Drd2 expression in Frontal Cortex - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		20													58.3		377.59		57.29		32.58		68.1		28.45		47.08		59.79						10.81										55.94				39.29				49.15		76.42		62.11				72.48		32.93																													M2D2FC							10591541.2
Drd2 expression in Frontal Cortex  - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		21											50.59		47.43		208		58.55		41.74		66.285		36.61		47.285		61.375						19.66										56.905				40.945		25.91		56.08		71.585		53.41				77.96		28.235																													MND2FC							10591541.21
Drd2 expression in ventral midbrain - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		22											49.61		0.95		53.95		24.64		58.46		62.65		48.91		41.17		58.22						32.54										61.37				47.44		42.6		46.8		74.43		39.58				44.64		45.91																													M1D2VM							10591541.22
Drd2 expression in ventral midbrain -  females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		23													60.23		60.42		27.86		49.09		59.08		49.41		35.56		68.84						15.55										54.8				43.12				43.83		62.18		34.95				78.16		52.76																													M2D2VM							10591541.23
Drd2 expression in ventral midbrain - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		24											49.61		30.59		57.185		26.25		53.775		60.865		49.16		38.365		63.53						24.045										58.085				45.28		42.6		45.315		68.305		37.265				61.4		49.335																													MND2VM							10591541.24
Dopamine transporter expression in Nucleus Accumbens - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		25											496.35		4820		2936.87		2956.52		3350.8		3311		1382.24		3887.1		3787.66						3367.63										4630				2679.06		4503.83		4407.5		5570		1485.2				4348		2008.5																													M1DAUTNA							10591541.25
Dopamine transporter expression in Nucleus Accumbens - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		26													4930		3283		4445.33		2548		2776.44		2480.13		2734.35		4749						1286.33										3560				4371		3269		3660.97		5320		278.63				6356.38		2748.93																													M2DAUTNA							10591541.26
Dopamine transporter expression in Nucleus Accumbens - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		27											496.35		4875		3109.935		3700.925		2949.4		3043.72		1931.185		3310.725		4268.33						2326.98										4095				3525.03		3886.415		4034.235		5445		881.915				5352.19		2378.715																													MNDAUTNA							10591541.27
Dopamine transporter Caudate Putamen - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		28											709.36		90		2787.62		2666.34		4228.58		7985		4698.77		3294.14		4768.66						1495.5										6940				6453.62		6741.93		6109.09		8323.33		1967.76				8400.96		4286																													M1DAUTCP							10591541.28
Dopamine transporter expression in Caudate Putamen - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		29													6540		7311		3667.55		6359		5249.45		4108.66		2649.03		7018						937.83										7050				5979		7065.5		5028.35		7356.67		2541.46				7281.01		4465.53																													M2DAUTCP							10591541.29
Dopamine transporter expression in Caudate Putamen - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		30											709.36		3315		5049.31		3166.945		5293.79		6617.225		4403.715		2971.585		5893.33						1216.665										6995				6216.31		6903.715		5568.72		7840		2254.61				7840.985		4375.765																													MNDAUTCP							10591541.3
Dopamine transporter expression in  Frontal Cortex - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		31											659.89		380.72		395.51		629.01		549.63		1093		721.69		730.29		1400.65						226.96										658				1639.37		1084.06		981.23		640.5		121.98				1351.14		793.1																													M1DAUTFC							10591541.31
Dopamine transporter expression in  Frontal Cortex - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		32													533.09		954.9		403.68		97.31		1232.51		472.13		1348.58		606.1						399.67										264				117		1211.12		659.24		440		400.29				1332.19		343.12																													M2DAUTFC							10591541.32
Dopamine transporter expression in Frontal Cortex - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		33											659.89		456.905		675.205		516.345		323.47		1162.755		596.91		1039.435		1003.375						313.315										461				878.185		1147.59		820.235		540.25		261.135				1341.665		568.11																													MNDAUTFC							10591541.33
Dopamine transporter expression in  ventral midbrain - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		34											47.51		376.11		250.61		422.72		346.32		172.3		198.34		124.21		1024.01						834.55										852				390		1083.4		900.86		304		185.13				824.58		324.7																													M1DAUTVM							10591541.34
Dopamine transporter in ventral midbrain - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		35													290.49		411.3		737.98		231.1		674.25		492.02		674.14		625.7						419.03										811				84.49		1745.31		350.21		645.33		113.77				942.05		466.97																													M2DAUTVM							10591541.35
Dopamine transporter expression in ventral midbrain - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		36											47.51		333.3		330.955		580.35		288.71		423.275		345.18		399.175		824.855						626.79										831.5				237.245		1414.355		625.535		474.665		149.45				883.315		395.835																													MNDAUTVM							10591541.36
Open Field Habituation - Difference Score cM distance traveled 0-5 min minus 26-30 min		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		37											3602		7970		2689		9260		7485		5825		7816		4720		7377		6725				4464		6348		5098				5746		5518				5811		3865		9888		10600		4914		5392		7645		9783																													DIFFBETA							10591541.37
Cocaine stereotypy - number of repeated movements 5 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		38											23.9		-12.0909		-0.4545		-3.6364		28.4		25		19.8182		-5.5455		32.1		8.4				5.3333		8.625		16				27.8		20.1				18.2222		28		29.3333		31.3		10.8		35.5		12.1818		16.2727																													NS1_5DF							10591541.38
Cocaine stereotypy - number of repeated movements 5 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		39											-6.8		-11.9		12.3		18		15.3636		34.75		22.4545		0.7		8.5		12.5				13.5				37.5				21.8333		18.6				15		34		52.3		30		17.8				-1.5		19.333																													NS2_5DF							10591541.39
Cocaine stereotypy - number of repeated movements 5 mg/kg cocaine ip (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		40											13.6667		-12		5.619		7.6522		21.5714		30.5714		21.1364		-2.5714		20.3		10.45				9.4167		8.625		26.75				25.5625		19.35				16.45		30.6667		39.7727		30.6842		14.3		35.5		5.6667		17.65																													NSS_5DF							10591541.4
Cocaine Open Field Activity - total distance 5 mg/kg cocaine (Difference from saline) - males 		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		41											2194.6		1093.73		653.27		255.13		2711.7		3715.22		1177.6		759.91		1904.4		2046.7				179.83		1372.88		2233.75				1512.5		1201.3				2041.89		1101.89		2742.33		2597.11		1795		2155		1690.27		1310.91																													TD1_5DF							10591541.41
Cocaine Open Field Activity - total distance 5 mg/kg cocaine (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		42											1835.8		2194.5		588.7		1351.08		1839.36		4055.36		2005.82		1197		1000.4		1543.22				1182.33				3846.25				2829.67		2100.9				2051.18		2692.25		3533.5		3915.33		2787.8				1762.7		1210.7																													TD2_5DF							10591541.42
Cocaine Open Field Activity - total distance 5 mg/kg cocaine (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		43											2075		1617.9		622.52		912.7		2254.76		3902.3		1611.43		968.05		1452.4		1808.21				681.08		1372.88		3040				2006.44		1651.1				2047		1850.29		3101.95		3256.22		2291.4		2155		1724.76		1263.19																													TDS_5DF							10591541.43
Cocaine activity - vertical rearing movements 5 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		44											-2		1.4545		1.6		2		-0.3333		-2.375		5		-5.7273		-7.5		-8.4				-1		-14		-7.5				-0.4		-4.4				0.4444		-3.1		-1.1667		0.5		-6.6		11.3333		-5.0909		10.5455																													VM1_5DF							10591541.44
Cocaine activity - vertical rearing movements 5 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		45											10		7.4		-14.1		6		11		1.5455		0.8182		-4		-5.7		-1				-2.8333				-14				-8		7.1				-3.2727		-7.2857		-1.4		1.5		-8.6				-7.2		4.5																													VM2_5DF							10591541.45
Cocaine activity - vertical rearing movements 5 mg/kg cocaine ip (Difference from saline) - mean males and females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		46											2.2857		4.2857		-6.25		4.087		5.9		-0.1053		2.901		-4.9048		-6.6		-4.7				-1.9167		-14		-10.75				-3.5294		1.35				-1.6		-4.8235		-1.2727		1		-7.6		11.3333		-6.0952		7.6667																													VMS_5DF							10591541.46
Cocaine stereotypy - number of movements 15 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		47											19.4545		3.6667		14.7		-0.7273		42.6		61.7		45.6364		7.3636		47.6154		16.9				10.5		19		25.5				70.7		62.9				68.4545		50		41.3		33.6364		2		77.333		86.8182		44																													NS1_15DF							10591541.47
Cocaine stereotypy - number of movements 15 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		48													-7.44		26.545		40.917		1000.417		86.1		79.5		-1.909		46.3		38.2				25				60.25				53.4		80.7				35.545		39.333		52.273		74.364		18				39.182		61.6																													NS2_15DF							10591541.48
Cocaine stereotypy - number of movements 15 mg/kg cocaine ip (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		49											19.4545		-1.8889		20.9048		21		74.1364		73.9		61.7619		2.7273		47.0435		27.55				17.0909		19		42.875				64.9333		71.8				52		44.6667		47.0476		54		8.4		77.333		63		52.381																													NSS_15DF							10591541.49
Cocaine Open Field Activity - total distance 15 mg/kg cocaine (Difference from saline)  - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		50											3579.18		6650.91		1774.6		3500.6		5088.82		7017.6		4368.64		5007		6213.31		4561.3				3574.83		5452.83		5496.25				6155.3		4326.5				5827.64		4063.4		11211		4230.36		4538		4457		5598.09		4223.64																													TD1_15DF							10591541.5
Cocaine Open Field Activity - total distance 15 mg/kg cocaine (Difference from saline)  - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		51													3512.2		3032.18		7606.27		8513.17		9589.56		6710.8		5271.17		4328		5476				3917.2				6116.5				3859		4828.8				5737.82		6150.22		9452		7746.27		1128.25				4944		4797.7																													TD2_15DF							10591541.51
Cocaine Open Field Activity - total distance 15 mg/kg cocaine (Difference from saline)  - males and females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		52											3579.18		5156.29		2433.33		5651.19		6875.43		8235.89		5483.95		5144.83		5393.61		5018.65				3730.45		5452.83		5806.38				5389.87		4577.65				5782.73		5051.89		10285.21		5988.32		3174.1		4457		5271.05		4497																													TDS_15DF							10591541.52
Cocaine activity - vertical rearing movements 15 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		53											-3.3		-6.5455		-11.3333		-0.3636		-3.5455		-19.125		-7.3636		-4.6364		-11.1538		-4.1				1.5		-2.5714		-6.75				-5		-7				-6.0909		-8.4		-3.7		-0.4		-8.3333		-18.8		-6.3636		-2.1																													VM1_15DF							10591541.53
Cocaine activity - vertical rearing movements 15 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		54													-1.4444		-9.2		-7.0909		-7.0833		-11.4		-7.9		-3.0833		-15.875		-4.5				-3.4				-7				-7		-14.1111				-5.5455		-8.6667		-1.2727		-9		-0.5				-9.6364		-8.4444																													VM2_15DF							10591541.54
Cocaine activity - vertical rearing movements 15 mg/kg cocaine ip (Difference from saline) - mean males and females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		55											2.2857		-4.25		-10.2105		-3.7273		-5.3913		-14.8333		-7.619		-3.8261		-12.9524		-4.3				-0.7273		-2.5714		-6.875				-5.6667		-10.3684				-5.8182		-8.5263		-2.4286		-4.9048		-5.2		-18.8		-8		-5.1053																													VMS_15DF							10591541.55
Cocaine stereotypy - number of movements 30 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		56											15.5566		3.8		20		39.6		54.818		71.667		47.5		36.909		81.75		33.778				3.25		41.333		32.25				37.571		59.818				51.385		69		68.727		68.222		18.833		82.2		50.5		109.091																													NS1_30DF							10591541.56
Cocaine stereotypy - number of movements 30 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		57											32.75		14		22.545		24		63.545		93.364		76.083		9.636		70		0.556				21.667				70.25				97.4		101.364				77.222		31.2		73.444		120.091						40.455		63.182																													NS2_30DF							10591541.57
Cocaine stereotypy - number of movements 30 mg/kg cocaine ip (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		58											20.8462		8.9		21.333		31.8		59.1818		83.6		63.0909		23.2727		76.4091		17.1667				11.1429		41.3333		51.25				80		80.5909				61.9545		51		70.85		96.75		18.83333		82.2		45.2381		86.1364																													NSS_30DF							10591541.58
Cocaine Open Field Activity - total distance 30 mg/kg cocaine (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		59											5138.78		7692.3		2523.3		9445.14		8038.09		6483.44		8598.8		4809.09		7829		6242.56				3394.13		6141.17		6317.75				5389.86		5089.25				6155.62		5855.36		11323.91		9137.43		6353.67		6395.2		7609.4		7896.2																													TD1_30DF							10591541.59
Cocaine Open Field Activity - total distance 30 mg/kg cocaine (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		60											4406.25		8029.9		2724.55		6993.56		7777.18		9570		6825.09		3844.36		3277.8		8067.14				4819				7586.5				7748.2		6778.27				6744.3		3145.89		9256.78		13633						7764.27		10213.09																													TD2_30DF							10591541.6
Cocaine Open Field Activity - total distance 30 mg/kg cocaine (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		61											4913.38		7861.1		2628.71		8066.13		7907.64		8181.05		7669.71		4326.73		7123.91		7040.81				4004.79		6141.17		6952.13				6372.5		5897.04				6411.57		4636.1		10393.7		11884.72		6353.67		6395.2		7690.52		9109.81																													TDS_30DF							10591541.61
Cocaine activity - vertical rearing movements 30 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		62											-9.25		-7.1111		-22.375		-4.4		1.4		-11.4444		-7.8		-3.4545		-15.1667		-10.6667				-1.875		-6.8333		-10				-4.8571		-15.4545				-1.6923		-11.8182		-3.2727		-3.1		-9.1667		-7.25		-8.1		-8.8182																													VM1_30DF							10591541.62
Cocaine activity - vertical rearing movements 30 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		63											-11.75		-10.11111		-10.81818		-12		1.81818		-13.54545		-9.16667		-0.72727		-10.6		-5.125				-2.66667		-8		-10.25				-2		-14				-6.3		-10.3		-12.22222		-11.72727		-12.33333		-27		-5.72727		-14.4																													VM2_30DF							10591541.63
Cocaine activity - vertical rearing movements 30 mg/kg cocaine ip (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		64											-10.0833		-8.6111		-15.6842		-8		1.619		-12.6		-8.5455		-2.0909		-13.0909		-13.2222				-2.2143		-6.8333		-10.125				-3.6667		-15.0952				-3.6957		-11.5		-7.3		-7.619		-9.1667		-7.25		-6.8571		-11.4762																													VMS_30DF							10591541.64
Cocaine stereotypy - number of movements 45 mg/kg cocaine ip (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		65											31.125		40.2727		12.08333		14.3636		83.2727		47.2727		30.9		14.7273		89.0833		16.9				1.5		28.375		45.25				36.5714		39.5455				18.2		51.3		79		55.6		16.8333		76.5		5.4		51.1111																													NS1_45DF							10591541.65
Cocaine stereotypy - number of movements 45 mg/kg cocaine ip (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		66											51.6		5.8		0.8182		31.2		50.75		58.5556		53		0.2222		74.7273		38.4				10.8				20.75				43.2		66.2				19.333		41.2		57.8		77.4		15.333				33.1818		46.4167																													NS2_45DF							10591541.66
Cocaine stereotypy - number of movements 45 mg/kg cocaine ip (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		67											39		23.8571		6.6957		22.381		69.5789		52.35		42.4762		8.2		82.2174		27.65				5.7273		28.375		33				39.3333		52.2381				18.8182		46.25		68.4		66.5		16.3333		76.5		19.9524		48.4286																													NSS_45DF							10591541.67
Cocaine Open Field Activity - total distance 45 mg/kg cocaine  (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		68											5167.88		8081.18		3118.17		7006.45		7651		9608.18		5561.9		5277.55		7793.67		5834.1				5273.83		4397.75		6007.75				4820.57		4210.73				4037.9		4716.67		9595.73		5946.67		5099.67		5787		6691.9		7125.5																													TD1_45DF							10591541.68
Cocaine Open Field Activity - total distance 45 mg/kg cocaine  (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		69											6258.8		6524.8		3339.09		7076.55		7885.44		7719.89		7430.18		3791.22		7100.36		7641.1				4305.6				5703				5240		5918.6				5297.77		4288.89		7085.9		9051.2		5508.67				7988.18		5792.83																													TD2_45DF							10591541.69
Cocaine Open Field Activity - total distance 45 mg/kg cocaine  (Difference from saline) - males and females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		70											5587.46		7340.05		3223.83		7041.5		7756.5		8758.45		6540.52		4608.7		7462.09		6737.6				4833.73		4397.75		5855.38				4995.33		5024				4750		4502.78		8400.57		7580.63		5236		5787		7370.9		6325.9																													TDS_45DF							10591541.7
Cocaine activity - vertical rearing movements 45 mg/kg cocaine ip  (Difference from saline) - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		71											-4		-10.2727		-12.6		-11.7273		-6.1818		-7.7273		-10.5		-4		-8.1667		-10.25				-4.6667		-13.5		-7.75				0.5714		-5.9				-2.7778		-11.5		-0.6364		-6.4		-3		-19		-8.1818		-9.5																													VM1_45DF							10591541.71
Cocaine activity - vertical rearing movements 45 mg/kg cocaine ip  (Difference from saline) - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		72											-5.5		-12.3		-27		-12.1667		0.375		-22.625		-7.4545		-12.2222		-19.6364		-11.3333				-4				-7.75				-0.4		-7				-8		-16.2		-10.3		-16.4		-11.3333				-16.9		-12.9167																													VM2_45DF							10591541.72
Cocaine activity - vertical rearing movements 45 mg/kg cocaine ip  (Difference from saline) - male and female mean		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		73											-4.5455		-11.2381		-19.8		-11.9565		-3.4211		-14		-8.9048		-7.7		-13.6522		-10.8235				-4.3636		-13.5		-7.75				0.1667		-6.45				-5.8636		-13.85		-5.2381		-11.4		-5.7778		-19		-11.8571		-11.55																													VMS_45DF							10591541.73
Cocaine Open Field Behavior - Total Distance Area Under Curve, 5 mg/kg cocaine, Saline Covariate		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		74											6344.1		5600.6		3904.9		5340.5		5714.2		7861.3		5091.8		4983.1		4877.1		5963.5				4240.7		6514.6		7005.2				5962.8		4785.9				5435.1		5873		6522.6		6735.3		6477.4		6479.8		5332.6		5263.8																													AARTDC5							10591541.74
Cocaine Open Field Behavior - Total Distance Area Under Curve, 15 mg/kg cocaine, Saline Covariate		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		75											8070.2		8952.4		6378.8		9327.2		10735.2		12173.5		9471.2		8978.4		9227.5		8828.8				7701.2		9170.7		9655.7				8873.1		8577				9751.9		8952.6		14268.4		9888.3		6628.1		8682.7		9204.5		8352.3																													AARTDC15							10591541.75
Cocaine Open Field Behavior - Total Distance Area Under Curve, 30 mg/kg cocaine, Saline Covariate		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		76											8966.9		11803.8		6140.4		12347.2		11570.5		11909.3		11419.9		8272.3		10733.8		11381.1				7682.1		9567		11022.5				10457		9480.2				10020.9		8494		13953.4		15114.6		10095.9		9632.3		11379.2		13001.7																													AARTDC30							10591541.76
Cocaine Open Field Behavior - Total Distance Area Under Curve, 45 mg/kg cocaine, Saline Covariate		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		77											10619.6		11321.9		6331.1		11605.6		11243		12728.1		9879		8835.7		10837.6		11773.3				8156.1		10098.4		10310.8				8823.8		8130.9				7990.5		8542.5		11679.6		11098.3		9591.9		10106.3		10914.4		10489.1																													AARTDC45							10591541.77
Cocaine Open Field Behavior - Center Time (Difference from saline) 5 mg/kg cocaine - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		85											-53.5		-64.18182		-75.6		-35.90909		-26.22222		-39.11111		-36.27273		-58.27273		-45.6		-30				-65.66667		-54.75		-91.66667				-30.5		0.2				-33		-12.5		-2.25		-0.14286		-12.8		26.4		-55.54545		-31.09091																													CT1_5DF							10591541.85
Cocaine Open Field Behavior - Center Time (Difference from saline) 5 mg/kg cocaine - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		86											-33.4		-56.5		-32.875		-16.41667		-60		-43.58333		-17.63636		-15		-33.9		-34.55556				10.33333		-17.33333		-25				-22.33333		44.375				-53.6		-50.5		-10.3		-1.8		-41.6		-30.5		-60		-44.9																													CT2_5DF							10591541.86
Cocaine Open Field Behavior - Center Time (Difference from saline) 15 mg/kg cocaine - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		87											-37.72727		-35.18182		-36.22222		-37.18182		-6		-22.2		-11		-24.54545		-23.76923		-25.8				-53.83333		-17.85714		-18				-20.6		39.8				-1.8		-48.22222		-13.66667		-66.63636		3.33333		19.5		-42.5		-57.09091																													CT1_15DF							10591541.87
Cocaine Open Field Behavior - Center Time (Difference from saline) 15 mg/kg cocaine - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		78											-52.33333		-69.2		67.1		-30.08333		-8.66667		-45.33333		-20.4		-37.81818		-12.4		-6				53.75		-42		-29				-42.2		38.9				-43.11111		-49.55556		4.9		-47.18182		12.75		26.33333		-80.2		-12.5																													CT2_15DF							10591541.78
Cocaine Open Field Behavior - Center Time (Difference from saline) 30 mg/kg cocaine - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		79											-11.11111		-64.1		1.11111		-7.5		1.09091		-41.44444		1.7		19.09091		6.75		-44.88889				25.71429		-4.16667		-37				-9.42857		11.54545				-26.92308		-47.90909		-1		-71.77778		-17.5		-15.6		-18.5		-45.36364																													CT1_30DF							10591541.79
Cocaine Open Field Behavior - Center Time (Difference from saline) 30 mg/kg cocaine - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		80											-58.25		-55.3		21.44444		-23.88889		32.63636		-92.45455		37.41667		-44.09091		-3		-37.88889				2.16667		8		-14.75				25.4		30.18182				-39.7		-73.6		-40.375		-74.5		0		44		-43.9		-63.27273																													CT2_30DF							10591541.8
Cocaine Open Field Behavior - Center Time (Difference from saline) 45 mg/kg cocaine - males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		81											-17.28571		-67.81818		63.4		-20		-5		-69.45455		-10.3		-30.63636		-4.08333		-31.7				-9.5		-16.75		-17.5				6.71429		55.18182				-53.5		-12.6		41.6		-32.9		20.33333		-8.5		0.09091		-61.55556																													CT1_45DF							10591541.81
Cocaine Open Field Behavior - Center Time (Difference from saline) 45 mg/kg cocaine - females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		82											-33.6		11.3		17.1		1.5		67.88889		-38.33333		36.63636		-26.44444		-10		-55.4				-12		-62.5		92.5				22		62.1				3.33333		-38.22222		-6.5		-47.7		-12		9		-2.2		-49.66667																													CT2_45DF							10591541.82
Open Field Habituation - Difference Score cM distance traveled 0-5 min minus 26-30 min - Males		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		83											3703		8768		2398		11354		6675		3863		9278		5540		7742		5381				4402		6348		5393				5415		5138				5527		6118		11639		7952		5848		5392		7660		8248																													DIFBETAM							10591541.83
Open Field Habituation - Difference Score cM distance traveled 0-5 min minus 26-30 min - Females		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		84											3303		7068		2961		7784		8209		7369		6527		3869		6799		8371				4770				4781				5942		5984				7237		1189		7814		12083		-3478				7618		11201																													DIFBETAF							10591541.84
Cortex Iron Levels Male		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.5													22.9				33.2		12.7				19.8		18		24.6		18.7				19.3										19.8				24.3				21.3		19.9		14.9				20.2		15.4																													FECXM							10591541.005
Cortex Iron Levels Female		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.51													25.8				15.4		27.4				19.9		17.9		15.3		22				21.3										19.8				23.7				21.2		24.8		19.3				20.3		13.9																													FECXF							10591541.0051
Caudate Putamen Iron Levels Male		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.52													13.9				16.5		15.7				21.9		13.7		16.5		12.1				18.5										22.6				19.8				20.9		26.2		18.7				18.7		17.1																													FECPM							10591541.0052
Caudate Putamen Iron Levels Female		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.53													15.9				19.2		15.3				21.6		14.8		13.7		23.7				18.7										19.8				21				17		21.9		17.6				18.2		14.1																													FECPF							10591541.0053
Nucleus Accumbens Iron Levels Male		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.54													20.1				24.8		15.5				26.8		19.8		25.6		19.6				26										25.9				22.8				22.9		22		22				19.9		20.6																													FENAM							10591541.0054
Nucleus Accumbens Iron Levels Female		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.55													18.8				26.1		19.1				32.4		22.2		14.7		27.1				24.3										23.4				24.6				20.7		30.1		24				22.8		20.1																													FENAF							10591541.0055
Midbrain Iron Levels male		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.56													15.1				17.2		19.1				29.4		15.6		20.7		17.5				29.3										35.1				36.8				33.6		29.9		15.5				17.9		16.6																													FEMBM							10591541.0056
Midbrain Iron Levels Female		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.57													14.2				18.3		17.1				38.4		14.4		15.7		16.4				29.3										33.2				35.9				29.6		36		17.5				20.7		17.2																													FEMBF							10591541.0057
Liver Iron Levels Male		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.58													94.7				105.2		116.6				145.2		121.8		126.9		92.8				99.3										114.4				112.2				103		105		172.3				132.7		205.7																													FELIVM							10591541.0058
Liver Iron Levels Female		We recently conducted a dose-response study of the effects of cocaine on several activity measures in the panel of BxD/Ty recombinant inbred mice. Animals were tested in an automated activity chamber over 2 days with i.p. saline on day 1 and i.p. cocaine on day 2, at one of four doses, 5, 15, 30 or 45 mg kg(-1). The monitor recorded total distance traveled, nosepokes in a holeboard, repeated movements and time spent by an individual in proximity to the centre of the apparatus. Dose-response curves for locomotor activation, i.e. the difference between cocaine and saline scores, showed that for all strains tested, scores increased 5-30 mg kg(-1). With few exceptions, locomotor activity at 45 mg kg(-1) was not significantly higher than that at 30 mg kg(-1). Repeated movement scores showed patterns similar to locomotor activity and nosepokes tended to be progressively inhibited by increasing doses of cocaine. Recombinant inbred strain mean distributions for all behaviours and at all doses exhibited continuous, rather than discrete variation, thus providing evidence of multiple-gene effects on cocaine-related behaviours. Quantitative trait loci (QTL) analysis pointed to several chromosomal locations associated with variations in cocaine-related behaviours and some are either identical or close to QTL reported by others. In separate groups of animals, densities of dopamine D1, and D2 receptors and dopamine uptake transporters were measured in the medial prefrontal cortex, caudate-putamen, nucleus accumbens and ventral midbrain. In all areas, all measures showed distributions consistent with polygenic influence and were associated with QTL. Of particular interest was our finding of a large segment on chromosome 15, which is related to dopamine receptor densities and cocaine-related behaviours.	Jones BC, Tarantino LM, Rodriguez LA, Reed CL, McClearn GE, Plomin R, Erwin VG.	Quantitative-trait loci analysis of cocaine-related behaviours and neurochemistry.	Pharmacogenetics	9(5)	607-617	Oct	1999		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10591541&dopt=Abstract	10591541		0.59													142.1				187.4		135				138.7		204.9		201.5		154.9				181.8										116.4				154.4				159		134.2		143				214.7		233.8																													FELIVF							10591541.0059
Proliferation of lin-Sca1++ cells responding to early-acting factors: kit ligand (KL), flt3 ligand (flt3L), thrombopoietin (TPO) [cell number]		Quantitative trait analysis may shed light on mechanisms regulating hematopoiesis in vivo. Strain-dependent variation existed among C57BL/6 (B6), DBA/2, and BXD recombinant inbred mice in the responsiveness of primitive progenitor cells to the early-acting cytokines kit ligand, flt3 ligand, and thrombopoietin. A significant quantitative trait locus was found on chromosome 2Êthat could not be confirmed in congenic mice, however, probably because of epistasis. Because it has been shown that alleles of unknown X-linked genes confer a selective advantage to hematopoietic stem cells in vivo in humans and in cats, we also analyzed reciprocal male D2B6F1 and B6D2F1 mice, revealing an X-linked locus regulating the responsiveness of progenitor and stem cells to early-acting factors. Among DBA/2, B6, and BXD recombinant inbred mice, correlating genetic variation was found in the absolute number and frequency of LinSca1++kit+ cells, which are highly enriched in hematopoietic progenitor and stem cells, and in the number of LinSca1++kit cells, a population whose biologic significance is unknown, suggesting that both populations are functionally related. Suggestive quantitative trait loci (QTLs) for the number of LinSca1++ cells on chromosomes 2,Ê4,Êand 7Êwere confirmed in successive rounds of mapping. The locus on chromosome 2Êwas confirmed in congenic mice. We thus demonstrated genetic variation in the response to cytokines critical for hematopoiesis in vivo and in the pool size of cells belonging to a phenotype used to isolate essentially pure primitive progenitor and stem cells, and we identified loci that may be relevant to the regulation of hematopoiesis in steady state.	Henckaerts E, Geiger H, Langer JC, Rebollo P, Van Zant G, Snoeck HW	Genetically determined variation in the number of phenotypically defined progenitor and stem cells and in their response to early-acting cytokines	Blood	99(11)	3947-3954	Jun	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010793&dopt=Abstract	12010793		01	6-8 wks	42	56	Female	3	cell number					240	0	1066	0	4369	2119	124	72	635	0	371	0	946	0	886	0	2599	0	1377	0	2946	0	3365	833	2874	0	1725	324			527	0	3533	0	1066	0	311	0	1293	0	515	0	4766	1508	1964	511			1293	0	443	0	1856	0			2527	983	299	0							419	0							6/5/2003	MK Sullivan	MK Sullivan										12010793.01
Concurrence of peripheral blood B220% [%]		Relative proportions of peripheral blood (PB) B lymphocytes (B220%) as well as CD4 (CD4%) and CD8 (CD8%) T lymphocytes differ significantly among inbred mouse strains: B220% is high in C57BL/6J (B6) and C57BR/cdJ, intermediate in BALB/cByJ (BALB) and DBA/2J (D2), and low in NOD/LtJ (NOD) and SJL/J (SJL) mice, whereas CD4% and CD8% are high in NOD and SJL mice and low in the other 4 strains. By following segregating genetic markers linked to these traits in (B6 x D2) recombinant inbred (BXD RI) mice, the study defined 2 quantitative trait loci (QTLs) for the B220% phenotype: Pbbcp1 (peripheral blood B cell percentage 1, logarithm of odds [LOD] 4.1, P <.000 01) and Pbbcp2 (LOD 3.7, P <.000 04) on chromosome 1 (Chr 1) at about 63 cM and 48 cM; one suggestive locus for the CD4% phenotype (LOD 2.6, P <.000 57) on Chr 8 at about 73 cM; and one QTL for the CD8% phenotype: Pbctlp1 (peripheral blood cytotoxic T lymphocyte percentage 1, LOD 3.8, P <.000 02) on Chr 19 at about 12 cM. The study further segregated PB lymphocyte proportions in B6SJLF2 mice by using DNA markers adjacent to these mapped QTLs and found that the Pbbcp1 locus (LOD 5.6, P <.000 01) was also important in this mouse population. In both BXD RI and B6SJLF2 mice, QTLs regulating B-cell proportions showed no significant effect on T-cell proportions and vice versa. Thus, PB B- and T-lymphocyte proportions are regulated separately by different genetic elements.	Chen J, Harrison DE	Quantitative trait loci regulating relative lymphocyte proportions in mouse peripheral blood	Blood	99(2)	561-566	Jan	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11781239&dopt=Abstract	11781239		01	3-5 months	90	150	Male	3-4	%					60		64		49		38		58		61		44		61		55		67		53		34		44		60		9		48		58		39		44		69		53 		56		52		49		61		46		58		46		42		54		44		43		49		63				50				6/9/2003	MK Sullivn	MK Sullivan										11781239.01
Concurrence of peripheral blood CD4% [%]		Relative proportions of peripheral blood (PB) B lymphocytes (B220%) as well as CD4 (CD4%) and CD8 (CD8%) T lymphocytes differ significantly among inbred mouse strains: B220% is high in C57BL/6J (B6) and C57BR/cdJ, intermediate in BALB/cByJ (BALB) and DBA/2J (D2), and low in NOD/LtJ (NOD) and SJL/J (SJL) mice, whereas CD4% and CD8% are high in NOD and SJL mice and low in the other 4 strains. By following segregating genetic markers linked to these traits in (B6 x D2) recombinant inbred (BXD RI) mice, the study defined 2 quantitative trait loci (QTLs) for the B220% phenotype: Pbbcp1 (peripheral blood B cell percentage 1, logarithm of odds [LOD] 4.1, P <.000 01) and Pbbcp2 (LOD 3.7, P <.000 04) on chromosome 1 (Chr 1) at about 63 cM and 48 cM; one suggestive locus for the CD4% phenotype (LOD 2.6, P <.000 57) on Chr 8 at about 73 cM; and one QTL for the CD8% phenotype: Pbctlp1 (peripheral blood cytotoxic T lymphocyte percentage 1, LOD 3.8, P <.000 02) on Chr 19 at about 12 cM. The study further segregated PB lymphocyte proportions in B6SJLF2 mice by using DNA markers adjacent to these mapped QTLs and found that the Pbbcp1 locus (LOD 5.6, P <.000 01) was also important in this mouse population. In both BXD RI and B6SJLF2 mice, QTLs regulating B-cell proportions showed no significant effect on T-cell proportions and vice versa. Thus, PB B- and T-lymphocyte proportions are regulated separately by different genetic elements.	Chen J, Harrison DE	Quantitative trait loci regulating relative lymphocyte proportions in mouse peripheral blood	Blood	99(2)	561-566	Jan	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11781239&dopt=Abstract	11781239		02	3-5 months	90	150	Male	3-4	%					20		9		25		18		14		14		18		16		12		6		16		19		11		10		25		13		19		15		20		11		11		10		15		16		7		12		12		20		18		16		21		18		19		11				12				6/9/2003	MK Sullivn	MK Sullivan										11781239.02
Concurrence of peripheral blood CD8% [%]		Relative proportions of peripheral blood (PB) B lymphocytes (B220%) as well as CD4 (CD4%) and CD8 (CD8%) T lymphocytes differ significantly among inbred mouse strains: B220% is high in C57BL/6J (B6) and C57BR/cdJ, intermediate in BALB/cByJ (BALB) and DBA/2J (D2), and low in NOD/LtJ (NOD) and SJL/J (SJL) mice, whereas CD4% and CD8% are high in NOD and SJL mice and low in the other 4 strains. By following segregating genetic markers linked to these traits in (B6 x D2) recombinant inbred (BXD RI) mice, the study defined 2 quantitative trait loci (QTLs) for the B220% phenotype: Pbbcp1 (peripheral blood B cell percentage 1, logarithm of odds [LOD] 4.1, P <.000 01) and Pbbcp2 (LOD 3.7, P <.000 04) on chromosome 1 (Chr 1) at about 63 cM and 48 cM; one suggestive locus for the CD4% phenotype (LOD 2.6, P <.000 57) on Chr 8 at about 73 cM; and one QTL for the CD8% phenotype: Pbctlp1 (peripheral blood cytotoxic T lymphocyte percentage 1, LOD 3.8, P <.000 02) on Chr 19 at about 12 cM. The study further segregated PB lymphocyte proportions in B6SJLF2 mice by using DNA markers adjacent to these mapped QTLs and found that the Pbbcp1 locus (LOD 5.6, P <.000 01) was also important in this mouse population. In both BXD RI and B6SJLF2 mice, QTLs regulating B-cell proportions showed no significant effect on T-cell proportions and vice versa. Thus, PB B- and T-lymphocyte proportions are regulated separately by different genetic elements.	Chen J, Harrison DE	Quantitative trait loci regulating relative lymphocyte proportions in mouse peripheral blood	Blood	99(2)	561-566	Jan 	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11781239&dopt=Abstract	11781239		03	3-5 months	90	150	Male	3-4	%					7.7		6.1		11.5		9.0		6.4		11.7		7.1		7.1		5.6		2.5		7.5		14.6		7.1		6.4		25.4		6.9		10.0		9.0		8.0		4.5		13.5		6.9		11.7		11.7		6.7		5.4		8.4		7.3		15.7		9.6		14.9		15.7		9.0		7.3				7.6				6/9/2003	MK Sullivn	MK Sullivan										11781239.03
Caudate putamen Drd2/3 receptor density binding of [125I] epidepride [fmol/mg]		BACKGROUND It has not been established to what extent the natural variation in dopamine systems contribute to the variation in ethanol response. The current study addresses this issue by measuring D dopamine (DA) receptor binding, the expression of, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of ethanol and other drug-related phenotypes.(2)METHODS Data were collected for 21 to 23 of the BXD RI strains and the parental strains. D DA receptor autoradiography was performed using I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025]. expression was measured using the Affymetrix oligoarray system. Immunocytochemical techniques were used to determine the number of midbrain DA neurons [Hitzemann B, Dains K, Hitzemann R (1994) Further studies on the relationship between dopamine cell density and haloperidol response. J Pharmacol Exp Ther 271:969-976].(2)RESULTS AND CONCLUSIONS The range of difference in receptor binding for the RI strains was approximately 2-fold in all regions examined, the core, the shell of the nucleus accumbens (NAc) and the dorsomedial caudate-putamen (CPu); heritability in all regions was moderate-( 2 approximately 0.35). expression in forebrain samples from the RI and parental strains ranged 1.5- to 2-fold and was moderate-0.47. Variation in the number of tyrosine hydroxylase (TH) positive neurons was moderate, 41% and 26% and was low-0.19 and 0.15 for the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Significant correlations were found between D DA receptor binding and the low dose (1.33 g/kg) ethanol stimulant response. ( < 0.002) and between expression and conditioned place preference (CPP) ( < 0.0005). No significant correlations were detected between ethanol preference and either receptor binding or expression; however, a significant correlation was found between preference and expression. is approximately 0.2 Mb from. Overall, the data suggest ethanol preference and CPP are associated with the expression of or closely linked genetic loci.(2)	Hitzemann R, Hitzemann B,  Rivera S, Gatley J, Thanos P, Siming Shou LL, Williams RW	Dopamine D2 receptor binding, Drd2 Expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to alcohol and other drug associated phenotypes	Alcohol Clin Exp Res	27(1)	1-11	Jan	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12543998&dopt=Abstract	12543998		01				Male	10-15	fmol/mg	311	17.7	304	20.9							278	62.9	295	44.6	253	29.4	250	50.3			263	29.4	261	18.6	240	34.3	213	30.0	267	20.6	268	27.4	235	23.7	175	37.7	235	58.9	263	32.3	238	54.0	167	35.4	269	27.1	264	52.9	218	32.6	295	59.4	281	70.9	199	22.6																																			12543998.01
Nucleus accumbens core Drd2/3 receptor density binding of [125I] epidepride [fmol/mg]		BACKGROUND It has not been established to what extent the natural variation in dopamine systems contribute to the variation in ethanol response. The current study addresses this issue by measuring D dopamine (DA) receptor binding, the expression of, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of ethanol and other drug-related phenotypes.(2)METHODS Data were collected for 21 to 23 of the BXD RI strains and the parental strains. D DA receptor autoradiography was performed using I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025]. expression was measured using the Affymetrix oligoarray system. Immunocytochemical techniques were used to determine the number of midbrain DA neurons [Hitzemann B, Dains K, Hitzemann R (1994) Further studies on the relationship between dopamine cell density and haloperidol response. J Pharmacol Exp Ther 271:969-976].(2)RESULTS AND CONCLUSIONS The range of difference in receptor binding for the RI strains was approximately 2-fold in all regions examined, the core, the shell of the nucleus accumbens (NAc) and the dorsomedial caudate-putamen (CPu); heritability in all regions was moderate-( 2 approximately 0.35). expression in forebrain samples from the RI and parental strains ranged 1.5- to 2-fold and was moderate-0.47. Variation in the number of tyrosine hydroxylase (TH) positive neurons was moderate, 41% and 26% and was low-0.19 and 0.15 for the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Significant correlations were found between D DA receptor binding and the low dose (1.33 g/kg) ethanol stimulant response. ( < 0.002) and between expression and conditioned place preference (CPP) ( < 0.0005). No significant correlations were detected between ethanol preference and either receptor binding or expression; however, a significant correlation was found between preference and expression. is approximately 0.2 Mb from. Overall, the data suggest ethanol preference and CPP are associated with the expression of or closely linked genetic loci.(2)	Hitzemann R, Hitzemann B,  Rivera S, Gatley J, Thanos P, Siming Shou LL, Williams RW	Dopamine D2 receptor binding, Drd2 Expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to alcohol and other drug associated phenotypes	Alcohol Clin Exp Res	27(1)	1-11	Jan	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12543998&dopt=Abstract	12543998		02				Male	10-15	fmol/mg	238	7.2	228	10.5							253	102.3	214	32.6	184	25.1	196	38.1			213	31.2	228	21.2	222	26.0	174	29.8	212	19.1	202	23.5	210	23.3	143	37.0	208	47.1	237	27.7	190	44.2	127	32.1	197	21.2	198	45.6	168	25.1	193	37.4	194	44.7	163	28.4																																			12543998.02
Nucleus accumbens shell Drd 2/3 receptor density binding of [125I] epidepride [fmol/mg]		BACKGROUND It has not been established to what extent the natural variation in dopamine systems contribute to the variation in ethanol response. The current study addresses this issue by measuring D dopamine (DA) receptor binding, the expression of, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of ethanol and other drug-related phenotypes.(2)METHODS Data were collected for 21 to 23 of the BXD RI strains and the parental strains. D DA receptor autoradiography was performed using I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025]. expression was measured using the Affymetrix oligoarray system. Immunocytochemical techniques were used to determine the number of midbrain DA neurons [Hitzemann B, Dains K, Hitzemann R (1994) Further studies on the relationship between dopamine cell density and haloperidol response. J Pharmacol Exp Ther 271:969-976].(2)RESULTS AND CONCLUSIONS The range of difference in receptor binding for the RI strains was approximately 2-fold in all regions examined, the core, the shell of the nucleus accumbens (NAc) and the dorsomedial caudate-putamen (CPu); heritability in all regions was moderate-( 2 approximately 0.35). expression in forebrain samples from the RI and parental strains ranged 1.5- to 2-fold and was moderate-0.47. Variation in the number of tyrosine hydroxylase (TH) positive neurons was moderate, 41% and 26% and was low-0.19 and 0.15 for the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Significant correlations were found between D DA receptor binding and the low dose (1.33 g/kg) ethanol stimulant response. ( < 0.002) and between expression and conditioned place preference (CPP) ( < 0.0005). No significant correlations were detected between ethanol preference and either receptor binding or expression; however, a significant correlation was found between preference and expression. is approximately 0.2 Mb from. Overall, the data suggest ethanol preference and CPP are associated with the expression of or closely linked genetic loci.(2)	Hitzemann R, Hitzemann B,  Rivera S, Gatley J, Thanos P, Siming Shou LL, Williams RW	Dopamine D2 receptor binding, Drd2 Expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to alcohol and other drug associated phenotypes	Alcohol Clin Exp Res	27(1)	1-11	Jan	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12543998&dopt=Abstract	12543998		03				Male	10-15	fmol/mg	268	8.5	242	17.9							264	89.1	223	36.8	181	32.3	195	40.3			206	31.5	213	28.8	216	27.5	171	34.1	203	26.7	196	23.5	212	30.7	144	38.9	210	48.0	239	30.9	179	44.0	128	22.9	189	25.6	181	48.8	173	25.3	186	43.2	187	46.7	161	17.8																																			12543998.03
Brain methamphetamine levels after 4 mg/kg methamphetamine [micrograms/gm]		Individual differences in most behavioral and pharmacological responses to abused drugs are dependent on both genetic and environmental factors. The genetic influences on the complex phenotypes related to drug abuse have been difficult to study using classical genetic analyses. Quantitative trait locus (QTL) mapping is a method that has been used successfully to examine genetic contributions to some of these traits by correlating allelic variation in polymorphic genetic markers of known chromosomal location with variation in drug-response phenotypes. We evaluated several behavioral responses to multiple doses of methamphetamine (METH) in C57BL/6J (B6), DBA/2J (D2), and 25 of their recombinant inbred (BXD RI) strains. Stereotyped chewing, horizontal home cage activity, and changes in body temperature after 0, 4, 8, or 16 mg/kg METH, as well as stereotyped climbing behavior after 16 mg/kg METH, were examined. Associations (p < 0.01) between METH sensitivity and allelic status at multiple microsatellite genetic markers were subsequently determined for each response. QTLs were provisionally identified for each phenotype, some unique to a particular behavior and others that appeared to influence multiple phenotypes. Candidate genes suggested by these analyses included several that mapped near genes relevant for the neurotransmitters acetylcholine and glutamate. The locations of QTLs provisionally identified by this analysis were compared with QTLs hypothesized in other studies to influence methamphetamine- and cocaine-related phenotypes. In several instances, QTLs appeared to overlap, which is consistent with idea that common neural substrates underlie some responses to psychostimulants.	Grisel JE, Belknap JK, O'Toole LA, Helms ML, Wenger CD, Crabbe JC. 	Quantitative trait loci affecting methamphetamine responses in BXD recombinant inbred mouse strains.	J Neurosci	17(2)	745-754	Jan 	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8987796&dopt=Abstract	8987796	98007483	11	10-14 wks	70	98	MF	8	micrograms/gm	0.5	0.12	0.8	0.17	1.1	0.26	0.5	0.12	0.7	0.10	0.7	0.14	0.9	0.22	0.5	0.13	0.5	0.17	0.8	0.29	0.8	0.11	1.1	0.28	0.9	0.17	0.5	0.15	0.2	0.07	0.8	0.25			0.6	0.10	0.6	0.21	0.7	0.20	0.5	0.14	0.5	0.10	0.8	0.30	0.5	0.13	0.4	0.11	0.4	0.10	1.4	0.33	0.8	0.26																							6/4/2003	MK Sullivan											8987796.11
54 degree C hot plate latencies baseline and post swim in maximum possible effect [%MPE=(postswim-baseline)/(cut-off-baseline)*100)]- MF [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	07	8-12 wks	56	96	MF	9-26	% MPE	68.7	9.50	52.2	10.20	95.0	3.23	34.3	8.42	74.3	10.70	78.6	6.54	79.5	8.81	90.4	6.52	83.6	7.33	82.9	6.98	100.0	0.63	41.6	10.00	64.3	8.19	77.0	7.46	77.2	7.88	40.1	6.80					6.28	14.91	50.3	8.75			86.5	7.08	87.2	5.29	79.2	7.35	39.8	8.83	41.9	10.80	25.5	8.25	59.5	7.00																							7/3/2003	MK Sullivan											9315917.07
54 degree C hot plate latencies baseline and post swim in maximum possible effect [%MPE=(postswim-baseline)/(cut-off-baseline)*100)]- Female [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	08	8-12 wks	56	96	Female	3-10	% MPE	67.8	9.50	47.2	10.20	95.3	3.23	26.2	8.42	81.5	10.70	80.0	6.54	83.8	8.81	86.2	6.52	88.2	7.33	82.3	6.98	99.7	0.63	33.8	10.00	55.2	8.19	77.7	7.46	68.7	7.88	43.9	6.80					40.3	14.91	41.2	8.75			94.0	7.08	99.7	5.29	71.4	7.35	38.5	8.83	28.3	10.80	5.6	8.25	65.9	7.00																							7/3/2003	MK Sullivan											9315917.08
54 degree C hot plate latencies baseline and post swim in maximum possible effect [%MPE=(postswim-baseline)/(cut-off-baseline)*100)]- Male [seconds]		It is increasingly appreciated that the sexes differ in their perception of noxious stimuli and in their responsivity to exogenous and endogenous analgesic manipulations. We previously reported the existence of qualitative sex differences in the neurochemical mediation of nonopioid (i.e., naloxone-insensitive) stress-induced analgesia (SIA) produced by forced swims and suggested that female mice possess a sex-specific SIA mechanism. This female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and to vary with reproductive status; however, its neurochemical identity remains obscure. In an attempt to identify candidate genes underlying SIA in both sexes, we performed a two-phase quantitative trait locus (QTL) mapping experiment using the BXD/Ty recombinant inbred (RI) set derived from DBA/2J (D2) and C57BL/6J (B6) inbred mouse strains and (B6xD2)F2 hybrid mice derived from these same progenitors. All mice were subjected to 3 min forced swims in 15 degrees C water; nociceptive sensitivity on the 54 degrees C hot-plate assay was assessed immediately before and 2 min after cessation of the swim. We report the localization of a QTL statistically associated with SIA magnitude [p = 0.00000012; logarithm of the odds (LOD) = 6.1] in female mice only. This female-specific QTL, which we name Fsia1, is located on chromosome 8 at 52-84 cM from the centromere and accounts for 17-26% of the overall trait variance in this sex. The present data provide further evidence of the existence of a female-specific SIA mechanism and highlight the important role of both genetic background and gender in the inhibition of pain.	Mogil JS, Richards SP, O'Toole LA, Helms ML, Mitchell SR, Kest B, Belknap JK.	Identification of a sex-specific quantitative trait locus mediating nonopioid stress-induced analgesia in female mice	J Neurosci	17(20)	7995-8002	Oct	1997		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315917&dopt=Abstract	9315917	97461641	09	8-12 wks	56	96	Male	4-18	% MPE	71.0	9.50	58.3	10.20	96.5	3.23	43.2	8.42	66.9	10.70	77.6	6.54	76.4	8.81	60.1	6.52	79.3	7.33	84.6	6.98	102.0	0.63	50.0	10.00	74.6	8.19	78.7	7.46	84.3	7.88	37.7	6.80					75.5	14.91	60.4	8.75			81.8	7.08	76.5	5.29	88.4	7.35	41.5	8.83	57.8	10.80	45.0	8.25	54.5	7.00																							7/3/2003	MK Sullivan											9315917.09
TRBV4+ T cell levels among CD8+ T cells in spleen [%]		The murine gamma-herpesvirus, MHV-68, shares important biological and genetic features with the human gamma-herpesvirus, Epstein-Barr virus. Following intranasal infection, mice develop an infectious mononucleosis-like syndrome accompanied by increased numbers of activated CD8+ T cells in the blood. A consistent feature of the CD8+ T-cell activation is a marked increase in the frequency of cells expressing a TRBV4+ T-cell receptor. Previous studies suggested that the magnitude of TRBV4 expansion varied significantly among mouse strains, and was influenced by both MHC and non-MHC genes. Detailed analysis of strains with high (C57BL/6) or low (DBA/2) TRBV4 CD8+ T-cell expansion showed that differences in the degree of expansion were not a consequence of variation in genetic susceptibility to the viral infection. Rather, the magnitude of the TRBV4 CD8+ T-cell expansion correlated with differences in expression of the unidentified stimulatory ligand on activated, latently infected B cells. In the present study, analysis of TRBV4 expansion in C57BL/6, DBA/2, B6D2 F1 mice, BXD recombinant inbred strains, and the progeny of C57BL/6xDBA/2 F1 hybrids backcrossed to C57BL/6 demonstrated strong cumulative dominance of the low DBA/2 trait and moderately high heritability (h2 approximately 0.5). Two quantitative trait loci (QTLs) strongly associated with variance in TRBV4 expansion were identified using simple and composite mapping procedures. The first QTL is located on Chromosome (Chr) 17, near or proximal to H2. The second QTL is located on Chr 6 in a region spanning the Tcrb and Cd8a loci.	Hardy CL, Lu L, Nguyen P, Woodland DL, Williams RW, Blackman MA	Identification of quantitative trait loci controlling activation of TRBV4 CD8+ cells during murine gamma-herpesvirus-induced infectious mononucleosis	Immunogenetics	53(5)	395-400	Jul	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11486276&dopt=Abstract	11486276		01	8-12 wks	56	84	Female		%	36.6	10.72	11.5	3.56	24.5	4.48	37.1	4.84	28.3	11.81	18.4	7.09	13.2	0	30.8	15.30	20.6	3.50	11.7	1.48	12.9	2.76	27.4	9.16	36.6	0	7.6	4.88	11.6	0.60	28.0	11.90			37.8	1.84	17.5	2.06	20.2	2.52	27.0	2.80	18.4	7.79	17.0	0.64	14.1	2.09	40.0	7.91	10.0	0.97	24.3	10.64	34.9	1.17																							6/18/2003	MK Sullivan	MK Sullivan										11486276.01
TRBV4+ T cell levels among CD*+ T cells in peripheral blood [%]		The murine gamma-herpesvirus, MHV-68, shares important biological and genetic features with the human gamma-herpesvirus, Epstein-Barr virus. Following intranasal infection, mice develop an infectious mononucleosis-like syndrome accompanied by increased numbers of activated CD8+ T cells in the blood. A consistent feature of the CD8+ T-cell activation is a marked increase in the frequency of cells expressing a TRBV4+ T-cell receptor. Previous studies suggested that the magnitude of TRBV4 expansion varied significantly among mouse strains, and was influenced by both MHC and non-MHC genes. Detailed analysis of strains with high (C57BL/6) or low (DBA/2) TRBV4 CD8+ T-cell expansion showed that differences in the degree of expansion were not a consequence of variation in genetic susceptibility to the viral infection. Rather, the magnitude of the TRBV4 CD8+ T-cell expansion correlated with differences in expression of the unidentified stimulatory ligand on activated, latently infected B cells. In the present study, analysis of TRBV4 expansion in C57BL/6, DBA/2, B6D2 F1 mice, BXD recombinant inbred strains, and the progeny of C57BL/6xDBA/2 F1 hybrids backcrossed to C57BL/6 demonstrated strong cumulative dominance of the low DBA/2 trait and moderately high heritability (h2 approximately 0.5). Two quantitative trait loci (QTLs) strongly associated with variance in TRBV4 expansion were identified using simple and composite mapping procedures. The first QTL is located on Chromosome (Chr) 17, near or proximal to H2. The second QTL is located on Chr 6 in a region spanning the Tcrb and Cd8a loci.	Hardy CL, Lu L, Nguyen P, Woodland DL, Williams RW, Blackman MA	Identification of quantitative trait loci controlling activation of TRBV4 CD8+ cells during murine gamma-herpesvirus-induced infectious mononucleosis	Immunogenetics	53(5)	395-400	Jul	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11486276&dopt=Abstract	11486276		02	8-12 wks	56	84	Female		%	44.5	11.96	11.4	1.84	29.3	5.58	27.8	15.83	32.4	10.72	27.9	10.81	18.4	3.18	24.7	12.61	18.9	3.78	15.5	1.80	10.9	3.54	15.6	5.84	33.4	0	34.3	5.10	11.2	3.26	32.5	10.90			17.6	4.80	21.5	1.48	23.0	3.47	32.0	4.16	21.6	10.96	19.6	1.44	8.5	2.16	30.2	5.58	12.2	1.47	26.3	13.0	39.4	0.71																							6/18/2003	MK Sullivan	MK Sullivan										11486276.02
Absolute number of lin-Sca1++ cells [cell number] 		Quantitative trait analysis may shed light on mechanisms regulating hematopoiesis in vivo. Strain-dependent variation existed among C57BL/6 (B6), DBA/2, and BXD recombinant inbred mice in the responsiveness of primitive progenitor cells to the early-acting cytokines kit ligand, flt3 ligand, and thrombopoietin. A significant quantitative trait locus was found on chromosome 2Êthat could not be confirmed in congenic mice, however, probably because of epistasis. Because it has been shown that alleles of unknown X-linked genes confer a selective advantage to hematopoietic stem cells in vivo in humans and in cats, we also analyzed reciprocal male D2B6F1 and B6D2F1 mice, revealing an X-linked locus regulating the responsiveness of progenitor and stem cells to early-acting factors. Among DBA/2, B6, and BXD recombinant inbred mice, correlating genetic variation was found in the absolute number and frequency of LinSca1++kit+ cells, which are highly enriched in hematopoietic progenitor and stem cells, and in the number of LinSca1++kit cells, a population whose biologic significance is unknown, suggesting that both populations are functionally related. Suggestive quantitative trait loci (QTLs) for the number of LinSca1++ cells on chromosomes 2,Ê4,Êand 7Êwere confirmed in successive rounds of mapping. The locus on chromosome 2Êwas confirmed in congenic mice. We thus demonstrated genetic variation in the response to cytokines critical for hematopoiesis in vivo and in the pool size of cells belonging to a phenotype used to isolate essentially pure primitive progenitor and stem cells, and we identified loci that may be relevant to the regulation of hematopoiesis in steady state.	Henckaerts E, Geiger H, Langer JC, Rebollo P, Van Zant G, Snoeck HW	Genetically determined variation in the number of phenotypically defined progenitor and stem cells and in their response to early-acting cytokines	Blood	99(11)	3947-3954	Jun	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010793&dopt=Abstract	12010793		02	6-8 wks	42	56	Female	3	cell number					3898	491	1469	316	5048	819	721	86	2798	261	2602	0	1348	0	3216	315	3864	0	5114	0	4468	807	3782	0	6832	0	1909	0			1508	0	3693	330	1489	0	983	0	852	0	2761	0	6472	447	1223	0			2000	0	4045	545	3180	0			2278	516	1563	0							2600	341							7/1/2003	MK Sullivan	MK Sullivan										12010793.02
Relative fraction of lin-Sca1++ cells [%]		Quantitative trait analysis may shed light on mechanisms regulating hematopoiesis in vivo. Strain-dependent variation existed among C57BL/6 (B6), DBA/2, and BXD recombinant inbred mice in the responsiveness of primitive progenitor cells to the early-acting cytokines kit ligand, flt3 ligand, and thrombopoietin. A significant quantitative trait locus was found on chromosome 2Êthat could not be confirmed in congenic mice, however, probably because of epistasis. Because it has been shown that alleles of unknown X-linked genes confer a selective advantage to hematopoietic stem cells in vivo in humans and in cats, we also analyzed reciprocal male D2B6F1 and B6D2F1 mice, revealing an X-linked locus regulating the responsiveness of progenitor and stem cells to early-acting factors. Among DBA/2, B6, and BXD recombinant inbred mice, correlating genetic variation was found in the absolute number and frequency of LinSca1++kit+ cells, which are highly enriched in hematopoietic progenitor and stem cells, and in the number of LinSca1++kit cells, a population whose biologic significance is unknown, suggesting that both populations are functionally related. Suggestive quantitative trait loci (QTLs) for the number of LinSca1++ cells on chromosomes 2,Ê4,Êand 7Êwere confirmed in successive rounds of mapping. The locus on chromosome 2Êwas confirmed in congenic mice. We thus demonstrated genetic variation in the response to cytokines critical for hematopoiesis in vivo and in the pool size of cells belonging to a phenotype used to isolate essentially pure primitive progenitor and stem cells, and we identified loci that may be relevant to the regulation of hematopoiesis in steady state.	Henckaerts E, Geiger H, Langer JC, Rebollo P, Van Zant G, Snoeck HW	Genetically determined variation in the number of phenotypically defined progenitor and stem cells and in their response to early-acting cytokines	Blood	99(11)	3947-3954	Jun	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010793&dopt=Abstract	12010793		03	6-8 wks	42	56	Female	3	%					0.376	0	0.149	0.028	0.747	0	0.128	0	0.438	0.057	0.277	0	0.201	0	0.352	0.070	0.579	0	0.460	0.120	0.316	0	0.495	0	0.600	0.126	0.201	0			0.189	0	0.606	0.035	0.297	0.039	0.165	0	0.201	0	0.270	0.072	0.652	0	0.180	0			0.379	0	0.738	0.146	0.579	0			0.264	0.077	0.229	0.040							0.338	0.066							7/1/2003	MK Sullivan	MK Sullivan										12010793.03
C-kit+ cells among lin-Sca1++ cells [%]		Quantitative trait analysis may shed light on mechanisms regulating hematopoiesis in vivo. Strain-dependent variation existed among C57BL/6 (B6), DBA/2, and BXD recombinant inbred mice in the responsiveness of primitive progenitor cells to the early-acting cytokines kit ligand, flt3 ligand, and thrombopoietin. A significant quantitative trait locus was found on chromosome 2Êthat could not be confirmed in congenic mice, however, probably because of epistasis. Because it has been shown that alleles of unknown X-linked genes confer a selective advantage to hematopoietic stem cells in vivo in humans and in cats, we also analyzed reciprocal male D2B6F1 and B6D2F1 mice, revealing an X-linked locus regulating the responsiveness of progenitor and stem cells to early-acting factors. Among DBA/2, B6, and BXD recombinant inbred mice, correlating genetic variation was found in the absolute number and frequency of LinSca1++kit+ cells, which are highly enriched in hematopoietic progenitor and stem cells, and in the number of LinSca1++kit cells, a population whose biologic significance is unknown, suggesting that both populations are functionally related. Suggestive quantitative trait loci (QTLs) for the number of LinSca1++ cells on chromosomes 2,Ê4,Êand 7Êwere confirmed in successive rounds of mapping. The locus on chromosome 2Êwas confirmed in congenic mice. We thus demonstrated genetic variation in the response to cytokines critical for hematopoiesis in vivo and in the pool size of cells belonging to a phenotype used to isolate essentially pure primitive progenitor and stem cells, and we identified loci that may be relevant to the regulation of hematopoiesis in steady state.	Henckaerts E, Geiger H, Langer JC, Rebollo P, Van Zant G, Snoeck HW	Genetically determined variation in the number of phenotypically defined progenitor and stem cells and in their response to early-acting cytokines	Blood	99(11)	3947-3954	Jun	2002		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010793&dopt=Abstract	12010793		04	8-10 wks	56	70	Female	3	%									22.1	0.91					25.0	10.52	0.6	0	19.9	0	20.8	0			17.0	4.02					16.0	0			24.2	0	11.5	0	29.0	0.91	20.4	5.98	29.6	5.42			30.5	5.76					37.6	4.55	27.3	0	19.7	3.18			1.74	0	10.6	3.33															7/1/2003	MK Sullivan	MK Sullivan										12010793.04
Adjusted cerebellum weight [mg] 		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		02	30-300 days	30	300	MF	4-7	mg					54.1	0.95	50.1	0.71	53.3	1.01	55.1	0.71	57.3	0.32	51.2	0.99	53.6	0.79	46.8	0.83	50.6	0.65	49.3	0.44	45.7	0.38	52.5	0.68	52.0	0.68	51.1	0.62	52.4	0.75	49.0	0.77	51.6	0.64	50.7	0.34	55.5	1.18	52.6	0.33	53.1	0.61	53.5	0.58	53.2	0.30	58.7	0.79	50.8	0.58	53.3	0.98	51.9	0.57	54.1	0.68	52.3	0.75	46.1	0.30			51.8	0.78	57.0	0.46	48.6	0.43			56.6	0.25			6/19/2003	MK Sullivan	MK Sullivan										11438585.02
Brain weight [mg]		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		03	30-300 days	30	300	MF	4-7	mg					483	20.3	403	8.6	501	13.0	403	5.0	438	22.9	448	9.6	408	5.8	405	16.9	392	12.9	414	6.6	437	14.2	450	6.8	429	11.9	409	15.9	374	13.3	437	8.7	435	12.3	394	8.1	408	9.6	385	4.9	359	16.2	394	4.3	385	4.5	365	6.2	403	8.5	439	6.0	445	3.0	439	5.2	417	14.4	427	6.3			436	9.6	423	5.3	455	8.2			469	7.0			6/19/2003	MK Sullivan	MK Sullivan										11438585.03
Cerebellum volume [mm3]		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		04	30-300 days	30	300	MF	4-8	mm3					49.8	2.32	45.5	1.23	62.9	3.55			55.1	1.64	47.3	1.10	50.6	1.21	43.8	1.75	47.9	1.18	47.1	1.71	44.5	0.87			47.5	2.23	46.4	1.16	43.2	0.96			50.4	1.47	43.1	1.21	50.7	3.52	45.1	1.05	43.5	2.00	47.7	1.90	40.9	2.35	47.9	2.11	46.0	1.81	55.1	3.66	48.2	3.13	50.4	2.85	46.9	1.96	40.9	1.29			45.5	2.46	50.6	1.64	44.9	3.90			53.4	1.37			6/19/2003	MK Sullivan	MK Sullivan										11438585.04
Adjusted cerebellum volume [mm3]		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		05	30-300 days	30	300	MF	4-8	mm3					46.0	1.89	44.9	1.42	52.5	3.41			54.3	1.87	45.8	1.02	49.0	1.01	42.6	1.30	48.3	1.09	45.0	1.64	41.6	0.80			47.8	2.06	45.8	0.64	45.8	0.83			48.0	1.03	43.9	1.61	52.2	3.52	46.6	0.75	49.3	1.44	49.3	1.93	46.0	1.31	52.6	1.47	46.8	2.04	51.5	3.28	47.7	3.61	51.0	2.10	48.2	1.19	42.5	0.87			45.8	2.00	52.6	0.41	44.2	3.87			51.1	1.01			6/19/2003	MK Sullivan	MK Sullivan										11438585.05
IGL volume [mm3]		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		06	30-300 days	30	300	MF	4-8	mm3					20.3	1.81	15.0	0.93	23.0	0.20			22.7	1.00	18.8	0.55	19.5	0.82	16.4	1.04	18.6	1.78	15.8	0.69	15.2	0.53			18.6	1.27	18.5	1.19	14.5	0.57			21.6	1.56	16.4	0.77	21.1	1.73	17.3	1.13	16.9	1.15	18.9	0.98	14.9	1.10	17.8	1.01	16.5	1.37	21.2	0.65	19.5	1.24	18.7	1.57	17.6	1.17	14.6	0.56			16.8	1.01	18.9	1.42	18.1	0.86			21.7	0.94			6/19/2003	MK Sullivan	MK Sullivan										11438585.06
Adjusted IGL volume [mm3]		To discover genes influencing cerebellum development, we conducted a complex trait analysis of variation in the size of the adult mouse cerebellum. We analyzed two sets of recombinant inbred BXD strains and an F2 intercross of the common inbred strains, C57BL/6J and DBA/2J. We measured cerebellar size as the weight or volume of fixed or histologically processed tissue. Among BXD recombinant inbred strains, the cerebellum averages 52 mg (12.4% of the brain) and ranges 18 mg in size. In F2 mice, the cerebellum averages 62 mg (12.9% of the brain) and ranges approximately 20 mg in size. Five quantitative trait loci (QTLs) that significantly control variation in cerebellar size were mapped to chromosomes 1 (Cbs1a), 8 (Cbs8a), 14 (Cbs14a), and 19 (Cbs19a, Cbs19b). In combination, these QTLs can shift cerebellar size an appreciable 35% of the observed range. To assess regional genetic control of the cerebellum, we also measured the volume of the cell-rich, internal granule layer (IGL) in a set of BXD strains. The IGL ranges from 34 to 43% of total cerebellar volume. The QTL Cbs8a is significantly linked to variation in IGL volume and is suggestively linked to variation in the number of cerebellar folia. The QTLs we have discovered are among the first loci shown to modulate the size and architecture of the adult mouse cerebellum.	Airey DC, Lu L, Williams RW.	Genetic control of the mouse cerebellum: identification of quantitative trait loci modulating size and architecture.	J Neurosci	21(14)	5099-5109	Jul	2001		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11438585&dopt=Abstract	11438585		07	30-300 days	30	300	MF	4-8	mm3					18.7	1.60	14.8	0.91	18.7	0.50			22.4	1.16	18.1	0.55	18.9	0.78	16.0	0.86	18.8	1.64	14.9	0.91	14.0	0.54			18.8	1.11	18.3	1.30	15.9	0.53			20.6	1.50	16.8	0.76	21.8	1.71	17.9	1.01	19.3	1.11	19.5	0.88	17.0	0.82	19.8	0.84	16.9	1.49	19.7	0.64	19.3	1.50	18.9	1.27	18.2	0.92	15.3	0.61			16.9	0.78	19.8	0.94	17.8	0.97			20.8	0.82			6/19/2003	MK Sullivan	MK Sullivan										11438585.07
Retinal ganglion cell number residual [cells x1000]		Common genetic polymorphisms-as opposed to rare mutations-generate almost all heritable differences in the size and structure of the CNS. Surprisingly, these normal variants have not previously been mapped or cloned in any vertebrate species. In a recent paper (), we suggested that much of the variation in retinal ganglion cell number in mice, and the striking bimodality of strain averages, are caused by one or two quantitative trait loci (QTLs). To test this idea, and to map genes linked to this variable and highly heritable quantitative trait, we have counted ganglion cells in 38 recombinant inbred strains (BXD and BXH) derived from parental strains that have high and low cell numbers. A genome-wide search using simple and composite interval-mapping techniques revealed a major QTL on chromosome (Chr) 11 in a 3 cM interval between Hoxb and Krt1 (LOD = 6.8; genome-wide p = 0.001) and possible subsidiary QTLs on Chr 2 and Chr 8. The Chr 11 locus, neuron number control 1 (Nnc1), accounts for one third of the genetic variance among BXH strains and more than half of that among BXD strains, but Nnc1 has no known effects on brain weight, eye weight, or total retinal cell number. Three strong candidate genes have been mapped previously to the same region as Nnc1. These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Each receptor is expressed in the retina during development, and their ligands affect the proliferation or survival of retinal cells.	Williams RW, Strom RC., Goldowitz D	Natural variation in neuron number in mice is linked to a major quantitative trait locus on Chr 11.	J Neurosci	18(1)	138-46	Jan	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9412494&dopt=Abstract	9412494	98075112	03	100 days	100		MF	5-11	cells x1000					-4.67		3.88		5.09		4.60		2.56		4.47		-1.47		-5.40		-6.88		1.08		0.79		-1.33		-6.48		5.16		0.91		-3.00		0.25		-9.20		4.03		-8.14		-7.75		-7.40		3.27		6.92		5.11		13.60																								6/18/2003	MK Sullivan	MK Sullivan										9412494.03
Tumor growth 2 weeks post-implantation [mm3]		Understanding of the genetic basis of normal and abnormal development of the immune response is an enormous undertaking. The immune response, at the most minimal level, involves interactions of antigen presenting cells (APCs), T and B cells. Each of these cells produce cell surface and soluble factors (cytokines) that affect both autocrine and paracrine functions. A second level of complexity needs to consider the development of the macrophage/monocyte lineage as well as the production of the common lymphoid precursor which undergoes distinct maturation steps in the thymus and periphery to form mature T cells as well as in BM (BM) and lymphoid organs to form mature B cells. A third level of complexity involves the immune response to infectious agents including viruses and also the response to tumour antigens. In addition, there are imbalances that predispose to decreased responses (immunodeficiencies) or increased responses (autoimmunity). A fourth level of complexity involves attempts to understand the differences in the immune response that occurs at a very young age, in adults, and at a very old age. This review will focus on the use of C57BL/6 J X DBA/2 J (BXD) recombinant inbred (RI) strains of mice to map genetic loci associated with the production of lymphoid precursors in the BM, development of T cells in the thymus, and T-cell responses to stimulation in the peripheral lymphoid organs in adult and in aged mice. Strategies to improve the power and precision in which complex traits such as the age-related immune response can be mapped is limited with the current set of 35 strains of BXD mice. Strategies to increase these strains by generating recombinant intercross (RIX) strains of mice are being developed to enable this large set of lines to detect quantitative trait loci (QTLs) with a much higher consistency and statistical power. More importantly, the resolution with which these QTLs can be mapped would be greatly improved and, in many cases, adequate to carry out direct identification of candidate genes. It is likely that, given the complexity of the immune system development, the number of cells involved in an immune response, and especially the changes in the immune system with ageing, mapping hundreds of genes will be required to fully understand age-related changes in the immune response. This review outlines ongoing and future strategies that will enable the mapping and identification of these genes.	Mountz JD, Van Zant GE, Zhang H-G, Grizzle WE, Ahmed R, Williams RW, Hsu H-C	Genetic dissection of age-related changes of immune function in mice	Scand J Immunol	54(1-2)	10-20	Jul-Aug	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11439143&dopt=Abstract	11439143		01	14 months	~426		MF		mm3									15.2						32.3		17.6		100.1																						52.4		29.9				41.1						145.8		33.0																								6/23/2003	MK Sullivan	MK Sullivan										11439143.01
Tumor growth 3 weeks post-implantation [mm3]		Understanding of the genetic basis of normal and abnormal development of the immune response is an enormous undertaking. The immune response, at the most minimal level, involves interactions of antigen presenting cells (APCs), T and B cells. Each of these cells produce cell surface and soluble factors (cytokines) that affect both autocrine and paracrine functions. A second level of complexity needs to consider the development of the macrophage/monocyte lineage as well as the production of the common lymphoid precursor which undergoes distinct maturation steps in the thymus and periphery to form mature T cells as well as in BM (BM) and lymphoid organs to form mature B cells. A third level of complexity involves the immune response to infectious agents including viruses and also the response to tumour antigens. In addition, there are imbalances that predispose to decreased responses (immunodeficiencies) or increased responses (autoimmunity). A fourth level of complexity involves attempts to understand the differences in the immune response that occurs at a very young age, in adults, and at a very old age. This review will focus on the use of C57BL/6 J X DBA/2 J (BXD) recombinant inbred (RI) strains of mice to map genetic loci associated with the production of lymphoid precursors in the BM, development of T cells in the thymus, and T-cell responses to stimulation in the peripheral lymphoid organs in adult and in aged mice. Strategies to improve the power and precision in which complex traits such as the age-related immune response can be mapped is limited with the current set of 35 strains of BXD mice. Strategies to increase these strains by generating recombinant intercross (RIX) strains of mice are being developed to enable this large set of lines to detect quantitative trait loci (QTLs) with a much higher consistency and statistical power. More importantly, the resolution with which these QTLs can be mapped would be greatly improved and, in many cases, adequate to carry out direct identification of candidate genes. It is likely that, given the complexity of the immune system development, the number of cells involved in an immune response, and especially the changes in the immune system with ageing, mapping hundreds of genes will be required to fully understand age-related changes in the immune response. This review outlines ongoing and future strategies that will enable the mapping and identification of these genes.	Mountz JD, Van Zant GE, Zhang H-G, Grizzle WE, Ahmed R, Williams RW, Hsu H-C	Genetic dissection of age-related changes of immune function in mice	Scand J Immunol	54(1-2)	10-20	Jul-Aug	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11439143&dopt=Abstract	11439143		02	14 months	~426		MF		mm3									11.6						11.7		2.7		62.7																						37.7		18.2				30.6						175.5		0																								6/23/2003	MK Sullivan	MK Sullivan										11439143.02
Tumor Growth 7 weeks post-implantation [mm3]		Understanding of the genetic basis of normal and abnormal development of the immune response is an enormous undertaking. The immune response, at the most minimal level, involves interactions of antigen presenting cells (APCs), T and B cells. Each of these cells produce cell surface and soluble factors (cytokines) that affect both autocrine and paracrine functions. A second level of complexity needs to consider the development of the macrophage/monocyte lineage as well as the production of the common lymphoid precursor which undergoes distinct maturation steps in the thymus and periphery to form mature T cells as well as in BM (BM) and lymphoid organs to form mature B cells. A third level of complexity involves the immune response to infectious agents including viruses and also the response to tumour antigens. In addition, there are imbalances that predispose to decreased responses (immunodeficiencies) or increased responses (autoimmunity). A fourth level of complexity involves attempts to understand the differences in the immune response that occurs at a very young age, in adults, and at a very old age. This review will focus on the use of C57BL/6 J X DBA/2 J (BXD) recombinant inbred (RI) strains of mice to map genetic loci associated with the production of lymphoid precursors in the BM, development of T cells in the thymus, and T-cell responses to stimulation in the peripheral lymphoid organs in adult and in aged mice. Strategies to improve the power and precision in which complex traits such as the age-related immune response can be mapped is limited with the current set of 35 strains of BXD mice. Strategies to increase these strains by generating recombinant intercross (RIX) strains of mice are being developed to enable this large set of lines to detect quantitative trait loci (QTLs) with a much higher consistency and statistical power. More importantly, the resolution with which these QTLs can be mapped would be greatly improved and, in many cases, adequate to carry out direct identification of candidate genes. It is likely that, given the complexity of the immune system development, the number of cells involved in an immune response, and especially the changes in the immune system with ageing, mapping hundreds of genes will be required to fully understand age-related changes in the immune response. This review outlines ongoing and future strategies that will enable the mapping and identification of these genes.	Mountz JD, Van Zant GE, Zhang H-G, Grizzle WE, Ahmed R, Williams RW, Hsu H-C	Genetic dissection of age-related changes of immune function in mice	Scand J Immunol	54(1-2)	10-20	Jul-Aug	2001		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11439143&dopt=Abstract	11439143		03	14 months	~426		MF		mm3									92.3						0		3.3		62.1																						26.9		0				26.9						856.7		0																								6/23/2003	MK Sullivan	MK Sullivan										11439143.03
Average distance traveled in thirty minutes, baseline [cm]		To elucidate genes associated with cocaine's locomotor stimulant effects, we used recombinant inbred-quantitative trait loci (RI-QTL) analyses to identify chromosomal loci associated with locomotor activity before (baseline) and after cocaine treatment. RI-QTL analyses seek to identify associations between a quantitative measure of a phenotype and one or more previously mapped marker loci across a panel of RI strains. In the present study, 11 BXD RI strains were used to identify several putative QTLs for each phenotype. Both baseline locomotor activity and cocaine's locomotor stimulant effects are polygenic, with both unique and overlapping genetic influences. The largest associations for baseline activity were observed on chromosomes 5 and 9 and the largest associations for cocaine's psychomotor stimulant effects on chromosomes 3 and 17.	Miner LL, Marley RJ	Chromosomal mapping of the psychomotor stimulant effects of cocaine in BXD recombinant inbred mice	Psychopharmacolgy	122(3)	209-214	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748389&dopt=Abstract	8748389		01	60-120 days	60	120	Male	6-15	cm	7281.6	504.9	8898.1	703.9	11964.4	1695.8			8103.6	1257.3	14430.4	1456.3			6556.6	1066.3	4687.7	491.9	8899.7	1537.2					8686.1	841.4	5096.9	550.2	10100.3	614.9															6022.7	749.2							6449.8	712.0																									6/24/2003	MK Sullivan	MK Sullivan										8748389.01
Average distance traveled in thirty minutes, cocaine-stimulated [cm]		To elucidate genes associated with cocaine's locomotor stimulant effects, we used recombinant inbred-quantitative trait loci (RI-QTL) analyses to identify chromosomal loci associated with locomotor activity before (baseline) and after cocaine treatment. RI-QTL analyses seek to identify associations between a quantitative measure of a phenotype and one or more previously mapped marker loci across a panel of RI strains. In the present study, 11 BXD RI strains were used to identify several putative QTLs for each phenotype. Both baseline locomotor activity and cocaine's locomotor stimulant effects are polygenic, with both unique and overlapping genetic influences. The largest associations for baseline activity were observed on chromosomes 5 and 9 and the largest associations for cocaine's psychomotor stimulant effects on chromosomes 3 and 17.	Miner LL, Marley RJ	Chromosomal mapping of the psychomotor stimulant effects of cocaine in BXD recombinant inbred mice	Psychopharmacolgy	122(3)	209-214	Dec	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8748389&dopt=Abstract	8748389		02	60-120 days	60	120	Male 	6-15	cm	7767.0	841.4	10920.7	1894.8	13071.2	1265.4			7896.4	1652.1	14561.5	1409.4			10946.6	2362.5	8200.6	1614.9	14453.1	2935.3					12119.7	2294.5	3038.8	823.6	10679.6	1508.1															4284.8	2411.0							5728.2	796.1																									6/24/2003	MK Sullivan	MK Sullivan										8748389.02
Stereotypical behavior frequency post daily cocaine injection (32 mg/kg), day 8		The present study investigated the effects of acute and repeated administration of cocaine (1.0-56.0 mg/kg) on locomotor activity in the genetically distinct DBA/2J and C57BL/6J inbred strains of mice. In addition, quantitative trait loci analysis of the effects of acute and repeated cocaine in 16 BXD recombinant inbred strains was used to provisionally detect and map minor gene loci which associate with cocaine responsiveness. Whereas locomotor activity was elevated maximally in both strains by 32 mg/kg of cocaine, DBA/2J mice were stimulated to a much greater extent than C57BL/6J mice. The stimulant effects of cocaine were diminished to control levels in DBA/2J mice after repeated daily injections, whereas cocaine-induced locomotion remained consistent in C57BL/6J mice throughout the 7-day testing period. Emergence of stereotyped behavior with repeated daily injections of 32 mg/kg of cocaine was observed in DBA/2J but not C57BL/6J mice. No differences in brain cocaine levels were found between the DBA/2J and C57BL/6J strains after acute or repeated injections. Quantitative trait loci analysis indicated significant associations of differences in cocaine responsiveness with marker loci on several chromosomes in the BXD recombinant inbred series. Those marker loci associated with the acute cocaine response were in most cases different from those markers associated with long-term responses. The current results demonstrate that genotype-dependent variation exists in behavioral responsiveness to cocaine in mice and suggest that the acute and long-term responses to cocaine may be under the control of separate sets of genes.	Tolliver BK, Belknap JK, Woods WE, Carney JM	Genetic analysis of sensitization and tolerance to cocaine	J Pharmacol Exp Ther	270(3)	1230-1238	Sep	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7932176&dopt=Abstract	7932176		03				Male	3-9		0.75	0.62	17.21	3.37					3.67	3.18			1.33	1.33			0.33	0.33			0.67	0.33	1.33	1.33	4.00	4.00	0.00	0.00							4.68	2.40	3.33	2.03	1.00	0.00			0.00	0.00	5.00	1.73	0.00	0.00			0.00	0.00	0.00	0.00	0.00	0.00																							6/26/2003	MK Sullivan											7932176.03
Average hypothermic response at 30 and 60 min post 2 g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		01	50-123 days	50	123	Female	4-14	degrees C	2.00	0.15	1.63	0.37	1.15	0.23	1.34	0.28	2.37	0.25	2.26	0.32	1.23	0.14	2.64	0.32			1.27	0.30	1.30	0.26	1.62	0.26	0.88	0.20	0.85	0.18	1.44	0.18					1.39	0.24	1.63	0.17			1.33	0.22	1.86	0.18	0.88	0.29	1.10	0.24	1.91	0.26																													6/23/2003	MK Sullivan	MK Sullivan										8169823.01
Average hypothermic response at 30 and 60 min post 3 g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		02	50-123 days	50	123	Female	4-14	degrees C	3.10	0.10	1.60	0.27	2.08	0.17	2.47	0.21	3.17	0.16	2.90	0.29	1.80	0.19	3.33	0.47			2.92	0.29	2.58	0.22	1.73	0.32	2.53	0.24	1.91	0.22	2.23	0.18					1.79	0.36	3.17	0.30			1.86	0.31	2.39	0.16	3.15	0.71	2.19	0.28	2.45	0.25																													6/23/2003	MK Sullivan	MK Sullivan										8169823.02
Average hypothermic response at 30 and 60 min post 4g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		03	50-123 days	50	123	Female	4-14	degrees C	3.40	0.14	2.93	0.48	2.33	0.14	2.53	0.24	3.65	0.20	3.48	0.21	2.11	0.18	3.47	0.54			2.98	0.34	3.73	0.54	3.90	0.40	3.23	0.35	1.83	0.19	2.71	0.43					2.74	0.23	2.77	0.25			2.40	0.52	2.07	0.23	4.29	0.30	2.31	0.18	2.92	0.13																													6/23/2003	MK Sullivan	MK Sullivan										8169823.03
Tolerance to ethanol-induced hypothermia post  2 g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		04	50-123 days	50	123	Female	4-14	degrees C	0.50	0.15	0.56	0.37	0.01	0.23	0.23	0.25	0.04	0.21	0.69	0.22	0.10	0.12	0.41	0.33			0.22	0.18	0.25	0.14	0.60	0.25	0.02	0.25	-0.05	0.19	-0.19	0.12					0.07	0.18	-0.50	0.21			-0.16	0.18	0.30	0.19	-0.11	0.38	-0.42	0.15	0.75	0.24																													6/23/2003	MK Sullivan	MK Sullivan										8169823.04
Tolerance to ethanol-induced hypothermia post 3 g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		05	50-123 days	50	123	Female	4-14	degrees C	0.91	0.17	-0.06	0.21	0.32	0.16	0.57	0.26	-0.02	0.18	0.44	0.24	0.18	0.26	0.69	0.34			0.70	0.28	0.16	0.23	-0.10	0.29	0.99	0.31	0.34	0.24	0.37	0.20					-0.73	0.31	0.18	0.25			-1.12	0.35	0.51	0.17	0.49	0.40	0.51	0.21	0.18	0.28																													6/23/2003	MK Sullivan	MK Sullivan										8169823.05
Tolerance to ethanol-induced hypothermia post  4 g/kg ethanol injection [degrees C]		A recent method allows the identification of the rough genetic map location in mice of genes that exert modest effects on continuously distributed (i.e., quantitative) variables. Sensitivity and tolerance tolerance to the hypothermic effect of ethanol were studied with the purpose of identifying such quantitative trait loci (QTL). Mice from two progenitor inbred strains, C57BL/6J and DBA/2J, and 19 of their recombinant inbred (RI) BXD strains, were given ethanol daily for 3 days. By administering several doses of ethanol and recording multiple postdrug temperatures on the first and third injection day, the authors were able to compute several indices of initial sensitivity and tolerance magnitude in the RI strain battery. The strains differed at most times and doses in their acute reductions in body temperature with respect to their predrug base lines, which indicated genetic control of sensitivity to ethanol-induced hypothermia. The areas under the curve (which describes the initial hypothermic response over time), a measure that reflects both the maximal hypothermia achieved and the duration of total hypothermic response, also differed. The strains also differed in the magnitude of the tolerance developed to ethanol-induced hypothermia. Genetic determinants of sensitivity (and tolerance) to different doses of ethanol were primarily independent, although genetic sensitivity and tolerance to the intermediate (2- and 3-g/kg) doses were significantly correlated. A comparison of the pattern of strain means for their sensitivity and tolerance to ethanol-induced hypothermia with a data base that consisted of the genotype of each BXD RI strain for almost 800 mapped polymorphic genetic markers revealed associations with several potential QTL for sensitivity and several others for tolerance, which appeared on all mouse chromosomes. Some QTL were significantly associated with both sensitivity and tolerance, which indicated that a nearby gene influences both. QTL analyses also identified several chromosomal regions in which specific candidate genes of potential relevance are mapped.	Crabbe JC, Belknap JK, Mitchell SR, Crawshaw LI	Quantitative trait loci mapping of genes that influence the sensitivity and tolerance to ethanol-induced hypothermia in BXD recombinant inbred mice 	J Pharmacol Exp Ther	269(1)	184-192	Apr 	1994		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8169823&dopt=Abstract	8169823		06	50-123 days	50	123	Female	4-14	degrees C	0.78	0.19	0.92	0.42	-0.10	0.20	0.35	0.32	0.68	0.30	0.86	0.24	-0.14	0.47	0.03	0.48			0.36	0.26	0.67	0.40	1.28	0.32	1.14	0.19	-0.11	0.16	0.47	0.34					0.50	0.14	0.34	0.28			-0.44	0.51	0.60	0.26	-0.72	0.37	0.57	0.35	0.38	0.20																													6/23/2003	MK Sullivan	MK Sullivan										8169823.06
Susceptibility to theiler's murine encephalomyelitis virus (TMEV) [% affected]		Theiler's virus-induced demyelinating disease results from a chronic infection in the white matter of the central nervous system and provides an excellent model for human multiple sclerosis. Like multiple sclerosis, there are genetic risk factors in disease development, including genes associated with the major histocompatibility complex and with those encoding the beta chain of the T-cell receptor. Comparisons of the susceptible DBA/2 and resistant C57BL/6 strains have indicated an important role for the H-2D locus and for a non-H-2 gene (not involving the beta chain of the T-cell receptor) in differential susceptibility. In the present report, analysis of recombinant-inbred strains (BXD) between the DBA/2 and C57BL/6 strains indicated that this non-H-2 locus is located at the centromeric end of chromosome 3 near (4 +/- 4 centimorgans) the carbonic anhydrase-2 (Car-2) enzyme locus.	Melvold RW, Jokinen DM, Miller SD, Del Canto MC, Lipton HL	Identification of a locus on mouse chromosome 3 involved in differential susceptibility to theiler's murine encephalomyelitis virus-induced demyelinating disease	J Virol	64(2)	686-690	Feb 	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2296080&dopt=Abstract	2296080 		01	4-6 wks	28	42	MF		% affected					56		11		73				11		63		84		100		0		0		0				53		10				0		10		0		93		10		88		0		0		67		89		20																								6/24/2003	MK Sullivan	MK Sullivan										2296080.01
Susceptibility to TMEV-induced demyelinating disease correlating with TMEV_specific DTH responsiveness [change in ear swelling (x10-4 in.)]		Theiler's virus-induced demyelinating disease results from a chronic infection in the white matter of the central nervous system and provides an excellent model for human multiple sclerosis. Like multiple sclerosis, there are genetic risk factors in disease development, including genes associated with the major histocompatibility complex and with those encoding the beta chain of the T-cell receptor. Comparisons of the susceptible DBA/2 and resistant C57BL/6 strains have indicated an important role for the H-2D locus and for a non-H-2 gene (not involving the beta chain of the T-cell receptor) in differential susceptibility. In the present report, analysis of recombinant-inbred strains (BXD) between the DBA/2 and C57BL/6 strains indicated that this non-H-2 locus is located at the centromeric end of chromosome 3 near (4 +/- 4 centimorgans) the carbonic anhydrase-2 (Car-2) enzyme locus.	Melvold RW, Jokinen DM, Miller SD, Del Canto MC, Lipton HL	Identification of a locus on mouse chromosome 3 involved in differential susceptibility to theiler's murine encephalomyelitis virus-induced demyelinating disease	J Virol	64(2)	686-690	Feb 	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2296080&dopt=Abstract	2296080 		02	118-162 days	118	162	MF		inches	4.2		16.9		12.4		4.3		16.1				10.0		19.2								4.9		7.7				22.1		0.2								0.9		32.8		3.5				2.4		6.5				17.4																										6/24/2003	MK Sullivan	MK Sullivan										2296080.02
Presence of VB3 lymph node T cells [%] 		V beta 3+ T cells are eliminated in Mls-2a mice carrying some, but not all, H-2 types. Analysis of AKXD and BXD recombinant inbred strains showed that Mls-2a (formerly Mlsc) was not the product of a single gene and suggested that at least two non-H-2 genes control V beta 3 levels. Studies of the progeny of a B10.BR x (C3H/HeJ x B10.BR)F1 backcross confirmed the existence of two V beta 3+ T cell deleting genes: one unlinked and one linked to Ly-7, which we propose be called Mls-2 and Mls-3, respectively. Mls-2a induces partial deletion of V beta 3+ T cells with a bias toward deleting CD4+ cells. It stimulates V beta 3+ hybrids and may be linked to Mtv-13 on chromosome 4. A third non-H-2 gene is implicated in enhancing the presentation of Mls-2a. Mls-3a causes elimination of all V beta 3+ T cells in H-2k and H-2d mice but poorly stimulates V beta 3+ hybrids.	Pullen AM, Marrack P, Kappler JW	Evidence that Mls-2anitgens which delete VB3+ T cells are controlled by multiple genes	J Immunol	142(9)	3033-3037	May 	1989		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2496158&dopt=Abstract	2496158 		01				MF		%	3.3	0.1	0.1	0.0	1.5	0.0	2.7	0.2	1.9	0.1	4.9	0.3	1.0	0.3	1.8	1.8	0.1	0.0	0.6	0.1	4.0	4.3	2.7	0.1	1.3	0.3	0.3	0.2	1.3	0.3	1.4	0.3			1.4	0.4	1.4	0.5	1.0	0.4	0.1	0.1	0.2	0.1	0.1	0.2	1.6	0.0	0.7	1.3	0.2	0.0																											6/24/2003	MK Sullivan	MK Sullivan										2496158.01
Proliferation of JTL-G12 (Tcell clone) without 50 µg/ml GAT (Glu60, Ala30, Tyr10) [cpm] 		We have isolated a BALB/c (H-2d, Mlsb) T cell clone (JTL-G12) specific for the synthetic polypeptide antigen poly(Glu60Ala30Tyr10) (GAT) in the context of self I-A determinants and for Mlsa,d antigens in the absence of GAT. JTL-G12 proliferation in response to GAT was mapped to the Kd, I-Ad subregions by using inbred H-2 congenic and recombinant strains. In addition, monoclonal antibody directed against I-Ad but not Kd or I-As determinants blocked JTL-G12 proliferation in response to GAT presented by syngeneic splenocytes, indicating I-A restriction. The Mls cross-reactivity of this clone was verified by using a panel of inbred strains bearing the Mlsa,b,c,d alleles and by using BXD recombinant inbred strains bearing the Mlsa allele or the Mlsb allele. All of the Mlsa BXD strains of the H-2d or H-2b haplotypes stimulated JTL-G12 in the absence of GAT, whereas all of the Mlsb BXD strains were nonstimulatory. This response pattern is in complete accordance with recognition of the Mlsa determinant encoded by Mls or closely linked loci on chromosome 1. JTL-G12 proliferation in response to GAT/I-Ad and Mlsa,d determinants could be blocked with a monoclonal antibody (GK1.5) directed against L3T4, a structure involved in class II major histocompatibility complex antigen recognition. These results suggest that antigen/class II responsiveness, Mls reactivity, and expression of L3T4 can be properties of a single T cell population.	Jenkins MK, Melvold RW, Miller SD	Isolation and characterization of an I-A-restricted T cell clone with dual specificity for poly (Glu60 Ala30 Tyr10) and MlsA,D1	J Immunol	133(2)	616-622	Aug	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6203970&dopt=Abstract	6203970 		01	6-10 wks	42	70	MF		cpm	410		10040		190		980		14010		120		10360		6050		7460		140		180		270		290		170		240		180				220		2260		140		6200		6750		8240		9110		6330		9920		290		6400																								7/15/2003	MK Sullivan	MK Sullivan										6203970.01
Proliferation of JTL-G12 (Tcell clone) with 50 µg/ml GAT (Glu60, Ala30, Tyr10) [cpm] 		We have isolated a BALB/c (H-2d, Mlsb) T cell clone (JTL-G12) specific for the synthetic polypeptide antigen poly(Glu60Ala30Tyr10) (GAT) in the context of self I-A determinants and for Mlsa,d antigens in the absence of GAT. JTL-G12 proliferation in response to GAT was mapped to the Kd, I-Ad subregions by using inbred H-2 congenic and recombinant strains. In addition, monoclonal antibody directed against I-Ad but not Kd or I-As determinants blocked JTL-G12 proliferation in response to GAT presented by syngeneic splenocytes, indicating I-A restriction. The Mls cross-reactivity of this clone was verified by using a panel of inbred strains bearing the Mlsa,b,c,d alleles and by using BXD recombinant inbred strains bearing the Mlsa allele or the Mlsb allele. All of the Mlsa BXD strains of the H-2d or H-2b haplotypes stimulated JTL-G12 in the absence of GAT, whereas all of the Mlsb BXD strains were nonstimulatory. This response pattern is in complete accordance with recognition of the Mlsa determinant encoded by Mls or closely linked loci on chromosome 1. JTL-G12 proliferation in response to GAT/I-Ad and Mlsa,d determinants could be blocked with a monoclonal antibody (GK1.5) directed against L3T4, a structure involved in class II major histocompatibility complex antigen recognition. These results suggest that antigen/class II responsiveness, Mls reactivity, and expression of L3T4 can be properties of a single T cell population.	Jenkins MK, Melvold RW, Miller SD	Isolation and characterization of an I-A-restricted T cell clone with dual specificity for poly (Glu60 Ala30 Tyr10) and MlsA,D1	J Immunol	133(2)	616-622	Aug	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6203970&dopt=Abstract	6203970 		02	6-10 wks	42	70	MF		cpm	270		11340		9420		2380		15850		12450		10080		10210		10480		14080		250		330		370		14690		17530		170				6330		6120		280		9820		11460		11810		13760		5480		14000		8150		7970																								7/15/2003	MK Sullivan	MK Sullivan										6203970.02
Proliferation of JTL-G12.8 (Tcell clone) without 50 µg/ml GAT (Glu60, Ala30, Tyr10) [cpm] 		We have isolated a BALB/c (H-2d, Mlsb) T cell clone (JTL-G12) specific for the synthetic polypeptide antigen poly(Glu60Ala30Tyr10) (GAT) in the context of self I-A determinants and for Mlsa,d antigens in the absence of GAT. JTL-G12 proliferation in response to GAT was mapped to the Kd, I-Ad subregions by using inbred H-2 congenic and recombinant strains. In addition, monoclonal antibody directed against I-Ad but not Kd or I-As determinants blocked JTL-G12 proliferation in response to GAT presented by syngeneic splenocytes, indicating I-A restriction. The Mls cross-reactivity of this clone was verified by using a panel of inbred strains bearing the Mlsa,b,c,d alleles and by using BXD recombinant inbred strains bearing the Mlsa allele or the Mlsb allele. All of the Mlsa BXD strains of the H-2d or H-2b haplotypes stimulated JTL-G12 in the absence of GAT, whereas all of the Mlsb BXD strains were nonstimulatory. This response pattern is in complete accordance with recognition of the Mlsa determinant encoded by Mls or closely linked loci on chromosome 1. JTL-G12 proliferation in response to GAT/I-Ad and Mlsa,d determinants could be blocked with a monoclonal antibody (GK1.5) directed against L3T4, a structure involved in class II major histocompatibility complex antigen recognition. These results suggest that antigen/class II responsiveness, Mls reactivity, and expression of L3T4 can be properties of a single T cell population.	Jenkins MK, Melvold RW, Miller SD	Isolation and characterization of an I-A-restricted T cell clone with dual specificity for poly (Glu60 Ala30 Tyr10) and MlsA,D1	J Immunol	133(2)	616-622	Aug	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6203970&dopt=Abstract	6203970 		03	6-10 wks	42	70	MF		cpm	160		4940		170		980		7470		160		7080		7000		5220		140		230		350		320		340		570		120				190		3290		140		4100		4240		5770		5310		2920		5590		590		4920																								7/15/2003	MK Sullivan	MK Sullivan										6203970.03
Proliferation of JTL-G12.8 (Tcell clone) with 50 µg/ml GAT (Glu60, Ala30, Tyr10) [cpm] 		We have isolated a BALB/c (H-2d, Mlsb) T cell clone (JTL-G12) specific for the synthetic polypeptide antigen poly(Glu60Ala30Tyr10) (GAT) in the context of self I-A determinants and for Mlsa,d antigens in the absence of GAT. JTL-G12 proliferation in response to GAT was mapped to the Kd, I-Ad subregions by using inbred H-2 congenic and recombinant strains. In addition, monoclonal antibody directed against I-Ad but not Kd or I-As determinants blocked JTL-G12 proliferation in response to GAT presented by syngeneic splenocytes, indicating I-A restriction. The Mls cross-reactivity of this clone was verified by using a panel of inbred strains bearing the Mlsa,b,c,d alleles and by using BXD recombinant inbred strains bearing the Mlsa allele or the Mlsb allele. All of the Mlsa BXD strains of the H-2d or H-2b haplotypes stimulated JTL-G12 in the absence of GAT, whereas all of the Mlsb BXD strains were nonstimulatory. This response pattern is in complete accordance with recognition of the Mlsa determinant encoded by Mls or closely linked loci on chromosome 1. JTL-G12 proliferation in response to GAT/I-Ad and Mlsa,d determinants could be blocked with a monoclonal antibody (GK1.5) directed against L3T4, a structure involved in class II major histocompatibility complex antigen recognition. These results suggest that antigen/class II responsiveness, Mls reactivity, and expression of L3T4 can be properties of a single T cell population.	Jenkins MK, Melvold RW, Miller SD	Isolation and characterization of an I-A-restricted T cell clone with dual specificity for poly (Glu60 Ala30 Tyr10) and MlsA,D1	J Immunol	133(2)	616-622	Aug	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6203970&dopt=Abstract	6203970 		04	6-10 wks	42	70	MF		cpm	210		7310		6580		1020		9040		9870		7000		9170		7120		8000		300		280		430		9150		9690		210				2600		4640		180		6240		7680		9580		7290		2560		8260		6410		5760																								7/15/2003	MK Sullivan	MK Sullivan										6203970.04
Morris water maze site preference [number of crosses over the trained site minus the mean of crosses over alternative sites] 		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		01	60-120 days	60	120	Male	3-13	number of crosses over the trained site minus the mean of crosses over alternative sites 					1.12	0.460	5.85	0.868							1.89	0.823									2.06	1.054	2.74	1.764							2.21	0.659			2.00	1.081	3.00	1.047	3.82	1.424	2.34	1.031	3.29	0.924																															6/24/2003	MK Sullivan	MK Sullivan										2400904.01
Morris water maze search-time preference, amount of time spent in the trained quadrant of the pool minus mean time in the alternative quadrants [seconds]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		02	60-120 days	60	120	Male	3-13	seconds					8.43	2.495	19.45	1.192							6.11	2.211									11.61	4.632	10.47	8.667							7.59	4.859			12.37	3.316	10.84	3.665	13.35	5.235	6.23	4.205	11.92	4.111																															6/24/2003	MK Sullivan	MK Sullivan										2400904.02
Protein kinase C (PKC) activity for total hippocampus [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		03	60-120 days	60	120	Male	3-9	pmol/min/mg protein					416	230.3	1347	145.3							568	132.0									398	64.2	901	112.5							856	91.9			844	110.1	1122	252.4	931	144.0	843	43.5	902	92.4																															6/24/2003	MK Sullivan	MK Sullivan										2400904.03
Protein kinase C (PKC) activity for particulate hippocampus [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		04	60-120 days	60	120	Male	3-9	pmol/min/mg protein					95	77.7	349	56.7							195	52.3									140	92.6	353	72.4							142	6.31			296	23.4	213	45.1	375	49.9	209	38.8	437	56.2																															6/24/2003	MK Sullivan	MK Sullivan										2400904.04
Protein kinase C (PKC) activity for cytosolic hippocampus [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		05	60-120 days	60	120	Male	3-9	pmol/min/mg protein					438	158.5	992	115.1							374	93.6									257	47.5	544	41.3							715	81.3			57.4	121.0	906	254.0	449	80.4	636	86.4	457	35.3																															6/24/2003	MK Sullivan	MK Sullivan										2400904.05
Protein kinase C (PKC) activity for total cortex [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		06	60-120 days	60	120	Male	3-9	pmol/min/mg protein					391	53.9	619	70.3							279	72.6									494	69.5	419	34.0							1018	155.4			273	108.1	503	60.6	356	41.4	495	156.5	540	124.2																															6/24/2003	MK Sullivan	MK Sullivan										2400904.06
Protein kinase C (PKC) activity for particulate cortex [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		07	60-120 days	60	120	Male	3-9	pmol/min/mg protein					184	27.6	177	43.2							113	44.6									295	129.2	142	54.6							560	167.2			154	147.2	137	56.5	67	105.7	259	109.9	194	87.0																															6/24/2003	MK Sullivan	MK Sullivan										2400904.07
Protein kinase C (PKC) activity for cytosolic cortex [pmol/min/mg protein]		Activation of protein kinase C (PKC) via neurotransmitter coupling processes has been associated with long-term potentiation (LTP) or classical conditioning, but whether natural variation in PKC activity affects learning performance remains to be determined. Inbred strains of mice differ in their ability to exhibit spatial reference memory as measured by the Morris water task. C57BL/6Ibg (C57) mice perform the task better than DBA/2Ibg (DBA) mice, which show relatively little spatial preference. Hippocampal PKC activity extracted from the particulate fraction was lower in DBA mice than in C57 mice. To examine the potential relationship of PKC activity with spatial learning performance, 11 C57BL/6J x DBA/2J recombinant inbred strains (BXD RIs) were trained in the place learning version of the Morris water task. Cortical and hippocampal PKC activities were measured. Variation in spatial learning performance and PKC activity from cortex and hippocampus was observed. A positive significant correlation was observed between measures of spatial learning accuracy and hippocampal PKC in these strains. No correlation was observed between spatial learning accuracy and cortical PKC activity. These data suggest that animals with lower hippocampal PKC activity may have problems performing spatial reference memory tasks with the same degree of accuracy as those with higher hippocampal PKC activity.	Wehner JM, Sleight S, Upchurch M	Hippocampal protein kinase C activity is reduced in poor spatial learners	Brain Res	523(2)	181-187	Jul	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2400904&dopt=Abstract	2400904		08	60-120 days	60	120	Male	3-9	pmol/min/mg protein					302	62.9	512	105.0							169	78.2									261	40.6	276	26.9							461	113.4			229	78.3	361	71.3	285	37.7	345	72.3	451	132.8																															6/24/2003	MK Sullivan	MK Sullivan										2400904.08
Anergy measured by footpad thickness resulting from BCG injection [mm]		The genetics of BCG-induced anergy was studied in mice by evaluating delayed hypersensitivity to sheep erythrocytes. Data obtained using congenic mice and by linkage analysis suggested that genes linked to the H-2 complex do not influence the development of anergy. However, studies in allotype-congenic partners (BALB/c; BALB.Igb) indicated that anergy was influenced by genes linked to the immunoglobulin heavy chain complex (Igh). Breeding studies indicated that the gene influencing anergy is recessive. These studies were extended by using BXD recombinant inbred mice, and verified that anergy is controlled by genes linked to the Igh complex. Because several markers and a tentative map has been constructed for the Igh complex on chromosome 12 in BXD mice, we suggest that the gene that controls BCG-induced anergy is located on the centrometric side of Igh-C approximately 18 to 28 recombination units.	Schrier DJ, Sternick JL, Allen EM, Moore VL	Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex	J Immunol	128(3)	1466-1469	Mar	1982		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6799576&dopt=Abstract	6799576 		01	8-12 wks 	56	84	MF	2-14	mm					0.68	0.11	0.22	0.08	0.25	0.06	0.67	0.14	0.14	0.03	0.63	0.11	0.64	0.02	0.79	0.04			0.15	0.05	0.48	0.14	0.92	0.06	0.92	0.07	0.15	0.03	0.86	0.08	1.0	0.17	0.31	0.03	0.30	0.12	0.60	0.07			0.74	0.11	0.80	0.13			0.99	0.08	0.46	0.08	0.64	0.07																							6/26/2003	MK Sullivan	MK Sullivan										6799576.01
Cerebellum fissure frequency (mean)		Variation in the cerebellar folial pattern of mice is influenced by genetic elements [Inouye, M. and Oda, S., J. Comp. Neurol., 190 (1980) 357-362]. In crosses of C57BL/6J and DBA/2J inbred mice, the presence or absence of a specific fissure, the intraculminate fissure, is largely determined by a single genetic locus (Cfp-1), which is located on distal Chromosome 4 [Neumann et al., Brain Res., 524 (1990) 85-89]. In the present study, the mid-sagittal cerebellar folial pattern has been examined in crosses of C57BL/6J and DBA/2J mice and in BXD recombinant inbred strains. At least three loci, including Cfp-1, are involved in variation in vermian pattern formation. Genetic variation in thyroid hormone function may be involved in the inheritance of folial pattern. A locus (Cfp-2) that appears to be partially responsible for this negative genetic correlation in mice may be linked to Afp on Chromosome 5. This hypothesis was suggested by the negative correlation between neonatal serum T4 level and the number of folia in rats given neonatal injections of thyroxine or propylthiouracil [Lauder, J.M. et al., Brain Res., 76 (1974) 33-40].	Neumann PE, Garretson JD, Skabardonis GP, Mueller GG	Genetic analysis  of cerebellar folial pattern in crosses of C57BL/6J and DBA?2J inbred mice	Brain Res	619(1-2)	81-88	Aug	1993			8374795		01					3-30	Fissure number					9.95	0.62	6.19	0.51	8.41	0.62	10.27	0.8	9.1	0.64	9.89	0.33	8.83	0.41	7.33	0.58	9.5	0.91	9.1	0.32	9.13	1.07	8.57	0.76	10.25	0.46	8.4	0.89	9.2	1.3	8.83	0.99	9.0	0.82	10.13	0.35	9.4	0.77	8.06	0.64	8.96	0.96	10.07	0.73	9.0	0.92	9.0	0.0	7.25	0.96	8.85	0.49																							6/24/2003	Mk Sullivan	Mk Sullivan										8374795.01
Ectromelia virus-induced mortality males [mortality number] 		Four genetic loci were tested for linkage with loci that control genetic resistance to lethal ectromelia virus infection in mice. Three of the loci were selected because of concordance with genotypes assigned to recombinant inbred (RI) strains of mice derived from resistant C57BL/6 and susceptible DBA/2 (BXD) mice on the basis of their responses to challenge infection. Thirty-six of 167 male (C57BL/6 x DBA/2)F1 x DBA/2 backcross (BC) mice died (22%), of which 27 (75%) were homozygous for DBA/2 alleles at Hc and H-2D. Twenty-eight percent of sham-castrated and 6% of sham-ovariectomized BC mice were susceptible to lethal mousepox, whereas 50% of gonadectomized mice were susceptible. There was no linkage evident between Hc or H-2D and loci that controlled resistance to lethal ectromelia virus infection in 44 castrated BC mice. Mortality among female mice of BXD RI strains with susceptible or intermediate male phenotypes was strongly correlated (r = 0.834) with male mortality. Gonadectomized C57BL/6 mice were as resistant as intact mice to lethal ectromelia virus infection. These results indicate that two gonad-dependent genes on chromosomes 2 and 17 and one gonad-independent gene control resistance to mousepox virus infection, that males and females share gonad-dependent genes, and that the gonad-independent gene is fully protective.	Brownstein DG, Bhatt PN, Gras L, Jacoby RO	Chromosomal locations and gonadal dependence of genes that mediate resistance to ectromelia (mousepox) virus-induced mortality	J Virol	65(4)	1946-1951	Apr	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2002550&dopt=Abstract	2002550		01	8 wks	56		Male	6-8	mortality number					3				8						7						4		3				6										2				8		5										4		8																								6/25/2003	MK Sullivan	MK Sullivan										2002550.01
Ectromelia virus-induced mortality females [mortality number]		Four genetic loci were tested for linkage with loci that control genetic resistance to lethal ectromelia virus infection in mice. Three of the loci were selected because of concordance with genotypes assigned to recombinant inbred (RI) strains of mice derived from resistant C57BL/6 and susceptible DBA/2 (BXD) mice on the basis of their responses to challenge infection. Thirty-six of 167 male (C57BL/6 x DBA/2)F1 x DBA/2 backcross (BC) mice died (22%), of which 27 (75%) were homozygous for DBA/2 alleles at Hc and H-2D. Twenty-eight percent of sham-castrated and 6% of sham-ovariectomized BC mice were susceptible to lethal mousepox, whereas 50% of gonadectomized mice were susceptible. There was no linkage evident between Hc or H-2D and loci that controlled resistance to lethal ectromelia virus infection in 44 castrated BC mice. Mortality among female mice of BXD RI strains with susceptible or intermediate male phenotypes was strongly correlated (r = 0.834) with male mortality. Gonadectomized C57BL/6 mice were as resistant as intact mice to lethal ectromelia virus infection. These results indicate that two gonad-dependent genes on chromosomes 2 and 17 and one gonad-independent gene control resistance to mousepox virus infection, that males and females share gonad-dependent genes, and that the gonad-independent gene is fully protective.	Brownstein DG, Bhatt PN, Gras L, Jacoby RO	Chromosomal locations and gonadal dependence of genes that mediate resistance to ectromelia (mousepox) virus-induced mortality	J Virol	65(4)	1946-1951	Apr	1991		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2002550&dopt=Abstract	2002550		02	8 wks	56		Female	7-8	mortality number					1				8						4						0		1				4										0				4		8										1		7																								6/25/2003	MK Sullivan	MK Sullivan										2002550.02
Life span (mean) [days] 		In this longevity analysis of 360 BXD recombinant inbred female mice (20 different strains), 2 strains had very significantly shorter survival and 1 strain had very significantly longer survival than the other 17 strains; 4 other strains had less significant lengthening of survival compared to the other 13 strains in a proportional hazards model of survival. Mean survival on the shortest lived strain was 479 days; on the longest lived strain the mean survival was almost double (904 days). Ranges of survival within strain were very large (averaging 642 days), and strain accounted for only 29% of the variation in survival, showing that there are important environmental and/or special developmental effects on longevity even in this colony housed in a single room. Each strain had been typed for markers of 141 regions on 15 chromosomes; 101 of these markers had distinguishable distributions on the 20 strains. The two shortest lived strains had the same alleles for 63% of the markers. The single region most significantly correlated with survival (marked by P450, Coh, Xmmv-35 on chromosome 7) divided the mice into two groups with survival medians which differed by 153 days (755 days for mice with a B genotype; 602 days for mice with a D genotype). Evaluated individually, 44% of the genetic markers (including some markers on 11 of 15 chromosomes with any markers typed) were found to be significantly correlated with survival (P less than 0.05) although one would only expect 5% of the markers to be significant by chance. While studies of many markers should adjust for the multiple comparisons problem, one interpretation of these crude P values is that any experiment with only one of these "significant" markers typed would be likely to conclude that the marker was a significant predictor of survival. Two types of multiple regression models were used to examine the correlation with survival of groups of genes. When a proportional hazards model for survival was done in terms of genotype regions, a six genetic region model best correlated with survival: that marked by P450, Coh, Xmmv-35 on chromosome 7 (B allele lives longer), Ly-24 on chromosome 2 (B allele lives longer), beta 2M and H-3 on chromosome 2 (D allele lives longer) Lamb-2 on chromosome 1 (D allele lives longer), Ltw-4 on chromosome 1 (B allele lives longer), and the Igh area of chromosome 12 (Igh-Sa4, Igh-Sa2, Igh-Bgl, Igh-Nbp, Igh-Npid, Igh-Gte, Odc-8, and Ox-1; D allele lives longer). A linear model that regressed mean survival (per strain) on genetic markers found a similar six region model to be best, but replaced Coh by D12Nyu1 on chromosome 12. It should be noted that in both types of regression, there were many other models almost as good as the best one. The total number of chromosomal regions marked by the genotype of the longer lived B parent (out of a possible 141) was not, in general, correlated with survival, although the two shortest lived strains had the most B genes. It appears that BXD recombinant inbred strains can vary widely in survival both within and between strains, that no single genetic marker which has yet been identified can account for much of this variance, (although groups of six or more markers may do so), and that it is not always those strains which inherit the most genes from the long-lived parent B that live longest. The large number of genetic markers found to be significantly correlated with survival raises questions of the reliability of conclusions based on survival studies of only one or two genetic regions. 	Gelman R, Watson A, Bronson R, Yunis E	Murine chromosomal regions correlated with longevity	Genetics	118(4)	693-704	Apr	1988		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3163317&dopt=Abstract	3163317		01				Female	10-21	days					594		479		528		687		617		816		750		738				493		798		642		742		904						743		763		835				711		765		703		737																												6/26/2003	MK Sullivan	MK Sullivan										3163317.01
Cytosolic Ah receptor levels in liver, fmol/mg cytosolic protein 		Aryl hydrocarbon (benzo[a]pyrene) hydroxylase inducibility by benzo[a]anthracene was studied in 29 somatic cell hybrid clones, developed by fusing mouse spleen or peritoneal cells from four different inbred strains with hypoxanthine phosphoribosyltransferase-deficient Chinese hamster E36 cells. Karyotype analysis plus 25 markers assigned to 16 autosomes and the X chromosome were examined. In 28 of the 29 clones, the presence or absence of inducibility is associated with the presence or absence, respectively, of mouse chromosome 17. Liver microsomal aryl hydrocarbon hydroxylase induction by 3-methylcholanthrene or benzo[a]anthracene was assessed in appropriate backcrosses with the Mus musculus molossinus, M. m. castaneus, MOR/Cv, PL/J, SM/J and DBA/2J inbred strains and in 13 NX8 recombinant inbred lines. Twenty-seven biochemical genetic markers representing all but four autosomes were tested for possible linkage with the hydroxylase inducibility, and no linkage was found. The hepatic Ah receptor was quantitated in 26 BXD recombinant inbred lines; the Ah phenotype did not match exactly any of the more than 70 genes with established strain distribution patterns representing 12 autosomes and at least five unlinked markers. It is concluded that a major gene controlling aryl hydrocarbon hydroxylase inducibility by benzo[a]anthracene is located on chromosome 17. Because there is no significant linkage with any of three biochemical markers in the upper third of the chromosome, we conclude that the inducibility gene is located in the distal 40% of mouse chromosome 17. Whether this trait represents the Ah locus, i.e., the gene encoding the cytosolic Ah receptor, will require further study.	Levgraverend C, Karenlampi SO, Bigelow SW, Lalley PA, Kozak CA, Womack JE, Nebert DW	Aryl hydrocarbon hydroxylase induction by benzo[a]anthracene: regulatory gene localized to the distal portion of mouse chromosome 17	Genetics	107(3)	447-461	Jul	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6547399&dopt=Abstract	6547399		01	5 wks  	35		MF	5	fmol/mg cytosolic protein 	38		0.5		57		0.5		9.0		50		46		1		39		1		43		66		1		12		65		1		2		0.5		1		1		0.5		60		1		2		42		41		0.5		0.5																								6/25/2003	MK Sullivan	MK Sullivan										6547399.01
XenCSA levels on thymus cells [mean flourescence value =sum of products of each channel number times the number of cells in that channel divided by the number of cells counted]		Rabbit antisera raised against rabbit corneal (SIRC) cells infected with xenotropic murine leukemia virus (MuLV)1 contain antibodies specific for antigens related to the major glycoproteins (gp70) of the xenotropic MuLV envelope (1). These antigens appear to be normal constituents of the cell surface of lymphocytes of all inbred mice and have been termed XenCSA-xenotropic MuLV envelope-related cell-surface antigens (1). The amount of XenCSA expressed on lymphocytes from various inbred strains differs greatly. Some strains, such as NZB, NZW, and DBA/2, express high levels of Xen CSA on both thymocytes and spleen cells whereas others, such as C57BL/6, NFS, and MA, express comparatively low levels of the antigen on both types of cells (1). To determine if quantitative expression of XenCSA is under genetic control, we have evaluated XenCSA levels in 24 recombinant inbred (RI) strains derived from crosses between DBA/2 and C57Bl/6 (2-7) as well as backcrosses of F1s to both parental strains. The results indicate that in this cross, Fv-1 or a closely linked gene on chromosome 4 has a major influence on XenCSA levels.  	Morse,III HC, Chused TM, Hartley JW, Mathieson BJ, Sharrow SO, Taylor BA	Expression of xenotropic murine leukemia viruses as cell-surface gp70 in genetic crosses between strains DBA/2 and C57BL/6	J Exp Med	149(5)	1183-1196	May 	1979		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=221612&dopt=Abstract	221612 		01	6-16 wks	42	112	MF	2-10	Mean flourescence value=sum of products of each channel number times the number of cells in that channel divided by the number of cells counted	80		160		111		67		96		118		95		74		62		114		216		328		109		227		131		80		71		101		63		70		62		133		126		160		65		146																												6/26/2003	MK Sullivan	MK Sullivan										221612.01
XenCSA levels on spleen cells [mean flourescence value =sum of products of each channel number times the number of cells in that channel divided by the number of cells counted]		Rabbit antisera raised against rabbit corneal (SIRC) cells infected with xenotropic murine leukemia virus (MuLV)1 contain antibodies specific for antigens related to the major glycoproteins (gp70) of the xenotropic MuLV envelope (1). These antigens appear to be normal constituents of the cell surface of lymphocytes of all inbred mice and have been termed XenCSA-xenotropic MuLV envelope-related cell-surface antigens (1). The amount of XenCSA expressed on lymphocytes from various inbred strains differs greatly. Some strains, such as NZB, NZW, and DBA/2, express high levels of Xen CSA on both thymocytes and spleen cells whereas others, such as C57BL/6, NFS, and MA, express comparatively low levels of the antigen on both types of cells (1). To determine if quantitative expression of XenCSA is under genetic control, we have evaluated XenCSA levels in 24 recombinant inbred (RI) strains derived from crosses between DBA/2 and C57Bl/6 (2-7) as well as backcrosses of F1s to both parental strains. The results indicate that in this cross, Fv-1 or a closely linked gene on chromosome 4 has a major influence on XenCSA levels.  	Morse,III HC, Chused TM, Hartley JW, Mathieson BJ, Sharrow SO, Taylor BA	Expression of xenotropic murine leukemia viruses as cell-surface gp70 in genetic crosses between strains DBA/2 and C57BL/6	J Exp Med	149(5)	1183-1196	May 	1979		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=221612&dopt=Abstract	221612 		02	6-16 wks	42	112	MF	2-10	Mean flourescence value=sum of products of each channel number times the number of cells in that channel divided by the number of cells counted	120		464		261		104		156		189		180		151		126		291		430		493		250		345		340		107		143		215		110		194		120		308		208		405		110		451																												6/26/2003	MK Sullivan	MK Sullivan										221612.02
Endogenous serum amyloid P-comonent (SAP) levels [µg/ml]		Recombinant inbred strains were used to demonstrate the existence of a major locus on chromosome 1, designated Sap, which controls the endogenous concentration of the mouse acute phase reactant, serum amyloid P-component (SAP). Levels of SAP were associated with alleles at the Ly-9 locus in two sets of RI strains: BXD (C57BL/6J X DBA/2) and BXH (C57BL/6J X C3H/HeJ). Low endogenous levels of SAP were present in the C57BL/6J progenitor strain and in most of the RI strains which inherited the Ly-9b allele. High levels of SAP were present in the DBA/2J and C3H/HeJ progenitors and in most of the RI strains which inherited the Ly-9a allele. In the BXD strains 91% of the genetic variation of SAP levels was accounted for by segregation at the Ly-9 locus while an additional 9% was attributed to genetic factors unlinked to Ly-9. In the BXH strains the percentage of genetic variation accounted for by Ly-9 segregation was reduced to 46%, while 54% was accounted for by other genetic factors. Because of background genetic variation it was not possible to detect any crossovers between Sap and Ly-9. However, in the BXD strains the linkage between Sap and Ly-9 appears to be quite close. The B6.C-H-25c congenic strain, which carries a segment of BALB/c chromosome 1 including the minor histocompatibility locus H-25 on a C57BL/6By background, had the same endogenous SAP level as the BALB/c donor strain.	Mortensen RF, Le PT, Taylor BA	Mouse serum amyloid p-component (SAP) levels controlled by a locus on chromosome 1	Immunogenetics	22(4)	367-375		1985		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4054960&dopt=Abstract	4054960		01	4-8 wks	28	42	MF	8-10	µg/ml	38.8	3.1	230.8	17.3	31.5	7.0	137.1	7.6	195.2	20.3	39.8	3.8	204.7	11.7	176.0	14.9	106.6	2.8	19.0	3.2	47.2	7.3	76.2	24.7	30.9	5.2	36.3	5.8	43.6	5.7	37.1	4.5			63.5	12.9	249.0	32.3	65.7	13.2	188.1	17.4	144.3	14.6	135.9	8.9	137.7	12.0	41.3	5.6	244.3	34.9	26.6	7.1	233.5	15.1																							6/26/2003	MK Sullivan	MK Sullivan										4054960.01
Audiogeneic seizure - relative frequency of seizures [%]		The difference in susceptibility to audiogenic seizures (AGS) between C57BL/6J and DBA/2J inbred strains of mice is due to multiple genetic factors. AGS susceptibility was tested in 21-day-old mice from classical crosses, BXD recombinant inbred (RI) strains, a congenic DBA/2N.B6N-Ahb inbred strain and crosses between the BXD RI strains and DBA/2J. Analysis of these data reveals that the variation in AGS susceptibility between these two strains results from allelic differences at three or more loci. Most of the variation is due to allelic differences at two loci. The first, Asp-1 (formerly Ias), is a major gene located on chromosome 12, between Ah and D12 Nyul. The second, Asp-2 (formerly asp), is a minor gene located on chromosome 4, tightly linked to b. The negative correlation of brain stem Ca2(+)-ATPase activity and AGS susceptibility in the BXD RI strains suggests that the strain difference in Ca2(+)-ATPase activity is inherited as a polygenic trait and that Asp-1 and Asp-2 are linked to, or identical to, factors that influence Ca2(+)-ATPase activity.	Neumann PE, Seyfried TN.	Mapping of two genes that influence susceptibility to audiogenic seizures in crosses of C57BL/6J and DBA/2J mice	Behav Genet 	20(2)	307-323	Mar	1990		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2141254&dopt=Abstract	2141254		02	20-22 days	20	22	MF	10-63	% of seizures	2		91		0		92		68		0		23		93		21		0		0		8		94		0		0		35				92				40		22		0		29		22		0		0				94																								6/26/2003	MK Sullivan	MK Sullivan										2141254.02
Red cell osmotic fragility [% lysis of red cells at 0.425% NaCl] 		Among normal mouse strains, natural genetic variation offers the potential to investigate the structure and function of cell membranes. One such polymorphism between C57BL/6J and DBA/2J is a difference in erythrocyte sensitivity to osmotic lysis. The genetic basis for erythrocyte osmotic fragility differences between mouse strains C57BL/6 and DBA/2 was examined through analyses of their serial backcross progeny, recombinant inbred (ri) strains (BXD), and congenic C57BL/6 strains with allelic differences at Hbb or Fv-2. The data indicate that the fragility difference between C57BL/6 and DBA/2 is the result of allelic differences at a minimum of two segregating loci. One of these might be linked to, but is not identical with the gene encoding the beta chain of hemoglobin (Hbb). Allelic differences at Fv-2, a gene known to control the proportion of erythroid precursors in the S phase, and at Hba, the structural locus of hemoglobin alpha chain also appear to exert no major influence on red cell osmotic fragility. Furthermore, the fact that red cells from one of the RI strans (BXD-31) are strikingly more resistant than those from the resistant parental strain DBA/2 leads to the conclusion that the degree of resistance/susceptibility for either strain is determined by the combined contributions of gene effects not all of which act in the same direction. We also found that red cells from strans C57BL/6 and DBA/2 differ in their uptake of 51Cr. This result suggests the possibility that red cell osmotic fragility differences may be due in part to differences in ion metabolism or membrane transport.	Norman NK, Dewey MJ	Genetic control of red cell osmotic fragility	J Hered	76(1)	31-35	Jan-Feb	1985		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3980972&dopt=Abstract	3980972		01	12-14	84	98	Female	2-5	%	59.8	6.85	16.1	1.92	51.8	2.11	43.7	13.07	30.8	4.91	40.0	3.74	35.9	5.72	23.9	7.94	42.9	5.85	17.9	5.67			34.1	8.64	16.0	5.71	50.8	7.21	32.9	5.07	48.0	5.00			27.0	2.76	40.0	5.79	22.1	5.67	30.7	2.93	33.1	4.00	57.6	7.00	37.0	4.80	36.0	3.69	30.0	7.86	8.00	7.89	32.1	5.00																							6/27/2003	MK Sullivan	MK Sullivan										3980972.01
Total ATPase activity [µmol Pi/h/mg protein]		Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.	Palayoor ST, Seyfried TN	Genetic study of cationic ATPase activities and audiogenic seizure  susceptibility in recombinant inbred and cogenic strains of mice	J Neurochem	42(2)	529-533	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6141222&dopt=Abstract	6141222 		01	20-22 days	20	22	MF	4-30	µmol Pi/h/mg protein	7.94	0.12	6.71	0.24	7.29	0.19	6.52	0.32	7.07	0.21	7.10	0.18			7.69	0.18	7.45	0.57	6.42	0.25	6.32	0.09			6.81	0.26	9.03	0.24											7.31	0.28							8.61	0.68	6.76	0.23																													6/27/2003	MK Sullivan	MK Sullivan										6141222.01
Mg2+ ATPase activity [µmol Pi/h/mg protein]		Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.	Palayoor ST, Seyfried TN	Genetic study of cationic ATPase activities and audiogenic seizure  susceptibility in recombinant inbred and cogenic strains of mice	J Neurochem	42(2)	529-533	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6141222&dopt=Abstract	6141222 		02	20-22 days	20	22	MF	4-30	µmol Pi/h/mg protein	4.66	0.10	3.34	0.12	3.78	0.15	3.72	0.12	4.01	0.27	3.90	0.16			3.58	0.24	4.31	0.17	3.64	0.28	3.66	0.24			3.71	0.32	5.02	0.16											4.16	0.34							4.60	0.31	4.45	0.25																													6/27/2003	MK Sullivan	MK Sullivan										6141222.02
Na+, K+ ATPase activity [µmol Pi/h/mg protein]		Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.	Palayoor ST, Seyfried TN	Genetic study of cationic ATPase activities and audiogenic seizure  susceptibility in recombinant inbred and cogenic strains of mice	J Neurochem	42(2)	529-533	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6141222&dopt=Abstract	6141222 		03	20-22 days	20	22	MF	4-30	µmol Pi/h/mg protein	3.28	0.11	3.37	0.14	3.51	0.20	2.92	0.39	3.06	0.31	3.20	0.19			4.11	0.36	3.14	0.42	2.79	0.38	2.66	0.26			3.10	0.22	4.01	0.23											3.15	0.13							4.01	0.43	2.31	0.13																													6/27/2003	MK Sullivan	MK Sullivan										6141222.03
Mean audiogenic seizure severity [severity of seizure]		Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.	Palayoor ST, Seyfried TN	Genetic study of cationic ATPase activities and audiogenic seizure  susceptibility in recombinant inbred and cogenic strains of mice	J Neurochem	42(2)	529-533	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6141222&dopt=Abstract	6141222 		04	20-22 days	20	22	MF	4-30	Severity of seizure; 0=no response, 1=wild running, 2=clonic or tonic seizure	0.07		1.89		0.20		1.92		1.64		0.14				1.85		1.04		0.30		0.09				1.78		0.21												1.16								1.00		0.09																														6/27/2003	MK Sullivan	MK Sullivan										6141222.04
Clonic-tonic audiogenic seizure susceptibility [%]		Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.	Palayoor ST, Seyfried TN	Genetic study of cationic ATPase activities and audiogenic seizure  susceptibility in recombinant inbred and cogenic strains of mice	J Neurochem	42(2)	529-533	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6141222&dopt=Abstract	6141222 		05	20-22 days	20	22	MF	4-30	%	1.8		91.4		0.0		92.0		68.0		0.0				93.0		21.0		0.0		0.0				82.2		0.0												40.0								22.0		0.0																														6/27/2003	MK Sullivan	MK Sullivan										6141222.05
Thymus to body size distribution [gmX103]		Differences exist among inbred mouse strains in the size of the thymus relative to overall body size. These differences are controlled by several genes acting in different phases of thymus development. After 50 days of age, there is an approximately 2-fold difference in thymus size between C57BL/6J and AKR/J, and other strains (A/J, DBA/2J, BALB/cJ, CBA/J, C3H/HeJ, 129/J, C57BL/ 10J , MA/ MyJ ). The C57BL/6J and AKR/J mice have the larger thymus, and this characteristic is dominant in F1 animals derived from C57BL/6J and A/J strains. Studies on recombinant inbred strains derived from C57BL/6J and DBA/2J ( BXD strains), and C57BL/6J and A/J ( AXB and BXA strains) indicate that this difference is controlled by alleles at one locus, which we have designated Tsz -1 (thymus size 1). In the immediate postnatal period (0-23 days), while the relative size of the thymus is increasing, the thymus size of C57BL/6J mice is large relative to that of A/J mice, but the A/J character is dominant during this period, and this difference appears to be controlled by two genes.	Peleg L, Nesbitt MN 	Genetic control of thymus size in inbred mice	J Hered	75(2)	126-130	Mar-Apr	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6715864&dopt=Abstract	6715864		01	55-100	55	100	Male		gm X103					1.80	0.491	0.82	0.423	1.10	0.402	1.72	0.388	0.91	0.205	1.70	0.200	1.14	0.139	1.11	0.293	1.72	0.533	0.95	0.242			1.10	0.494	0.90	0.202	2.17	0.587			1.05	0.243	1.20	0.335			1.12	0.335							1.25	0.238	1.16	0.588	1.82	0.429	1.22	0.487																							7/7/2003	MK Sullivan	MK Sullivan										6715864.01
Proliferation of A9.4 (subclone) without 50 µg/ml KLH experiment 1 [cpm]		A T cell clone isolated from antigen-primed CB6/F1 mice was shown to proliferate to keyhole limpet hemocyanin (KLH) in the presence of irradiated syngeneic F1 spleen cells, as well as spleen cells from either parental strain (BALB/c and C57BL/6). The genetic restriction involved in this antigen-specific proliferation was mapped using BXD (C57BL/6 X DBA/2) recombinant inbred strains of mice to the Mls gene on chromosome one. To exclude the role of Ia antigens as the restricting determinants, monoclonal anti-Ia antibodies were used to block the in vitro proliferative response of this clone. Although anti-Iab and anti-Iad blocked the proliferation of this clone to KLH in the presence of irradiated spleen cells from either parent, this effect was shown to be dependent on Ia molecules passively absorbed by the T cell clone from the irradiated filler cells. Since the T clone expressed Thy-1.2 and Lyt-1+ differentiation markers, its helper activity was compared with other KLH carrier-specific clones in an in vitro antibody synthesis assay. The Mls-KLH-restricted T cell clone, in contrast to other carrier-specific, major histocompatibility complex (MHC)-restricted T cell clones, was unable to cooperate with trinitrophenyl (TNP)-primed B cells in the presence of TNP-KLH to generate an anti-TNP response. These experiments suggest that non-MHC determinants, such as autologous Mls gene products, may play a role in genetically restricted antigen recognition by T lymphocytes.	Waters SJ, Waksal SD, Norton GP, Bona CA	Antigen recognition by a t cell clone outside the context of the major histocompatibility complex	J Exp Med	159(1)	305-312	Jan	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6198425&dopt=Abstract	6198425 		01	6-8 wks	42	56	MF		cpm 	1107	77	925	71	2021	148	158	23			2267	340	108	16					1757	128																					127	49							158	12																													6/30/2003	MK Sullivan	MK Sullivan										6198425.01
Proliferation of A9.4 (subclone) with 50 µg/ml KLH experiment 1, 5X105 stimulator cells [cpm] 		A T cell clone isolated from antigen-primed CB6/F1 mice was shown to proliferate to keyhole limpet hemocyanin (KLH) in the presence of irradiated syngeneic F1 spleen cells, as well as spleen cells from either parental strain (BALB/c and C57BL/6). The genetic restriction involved in this antigen-specific proliferation was mapped using BXD (C57BL/6 X DBA/2) recombinant inbred strains of mice to the Mls gene on chromosome one. To exclude the role of Ia antigens as the restricting determinants, monoclonal anti-Ia antibodies were used to block the in vitro proliferative response of this clone. Although anti-Iab and anti-Iad blocked the proliferation of this clone to KLH in the presence of irradiated spleen cells from either parent, this effect was shown to be dependent on Ia molecules passively absorbed by the T cell clone from the irradiated filler cells. Since the T clone expressed Thy-1.2 and Lyt-1+ differentiation markers, its helper activity was compared with other KLH carrier-specific clones in an in vitro antibody synthesis assay. The Mls-KLH-restricted T cell clone, in contrast to other carrier-specific, major histocompatibility complex (MHC)-restricted T cell clones, was unable to cooperate with trinitrophenyl (TNP)-primed B cells in the presence of TNP-KLH to generate an anti-TNP response. These experiments suggest that non-MHC determinants, such as autologous Mls gene products, may play a role in genetically restricted antigen recognition by T lymphocytes.	Waters SJ, Waksal SD, Norton GP, Bona CA	Antigen recognition by a t cell clone outside the context of the major histocompatibility complex	J Exp Med	159(1)	305-312	Jan	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6198425&dopt=Abstract	6198425 		02	6-8 wks	42	56	MF		cpm 	3457	137	3736	341	4568	302	209	140			5070	137	148	50					3990	97																					381	106							86	45																													6/30/2003	MK Sullivan	MK Sullivan										6198425.02
Proliferation of A9.4 (subclone) without 50 µg/ml KLH experiment 2 [cpm]		A T cell clone isolated from antigen-primed CB6/F1 mice was shown to proliferate to keyhole limpet hemocyanin (KLH) in the presence of irradiated syngeneic F1 spleen cells, as well as spleen cells from either parental strain (BALB/c and C57BL/6). The genetic restriction involved in this antigen-specific proliferation was mapped using BXD (C57BL/6 X DBA/2) recombinant inbred strains of mice to the Mls gene on chromosome one. To exclude the role of Ia antigens as the restricting determinants, monoclonal anti-Ia antibodies were used to block the in vitro proliferative response of this clone. Although anti-Iab and anti-Iad blocked the proliferation of this clone to KLH in the presence of irradiated spleen cells from either parent, this effect was shown to be dependent on Ia molecules passively absorbed by the T cell clone from the irradiated filler cells. Since the T clone expressed Thy-1.2 and Lyt-1+ differentiation markers, its helper activity was compared with other KLH carrier-specific clones in an in vitro antibody synthesis assay. The Mls-KLH-restricted T cell clone, in contrast to other carrier-specific, major histocompatibility complex (MHC)-restricted T cell clones, was unable to cooperate with trinitrophenyl (TNP)-primed B cells in the presence of TNP-KLH to generate an anti-TNP response. These experiments suggest that non-MHC determinants, such as autologous Mls gene products, may play a role in genetically restricted antigen recognition by T lymphocytes.	Waters SJ, Waksal SD, Norton GP, Bona CA	Antigen recognition by a t cell clone outside the context of the major histocompatibility complex	J Exp Med	159(1)	305-312	Jan	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6198425&dopt=Abstract	6198425 		03	6-8 wks	42	56	MF		cpm 	3765	805			4902	197	511	116			4413	328	593	419					2941	786																					158	67							248	121																													6/30/2003	MK Sullivan	MK Sullivan										6198425.03
Proliferation of A9.4 (subclone) with 50 µg/ml KLH experiment 2, 1X106 stimulator cells [cpm]		A T cell clone isolated from antigen-primed CB6/F1 mice was shown to proliferate to keyhole limpet hemocyanin (KLH) in the presence of irradiated syngeneic F1 spleen cells, as well as spleen cells from either parental strain (BALB/c and C57BL/6). The genetic restriction involved in this antigen-specific proliferation was mapped using BXD (C57BL/6 X DBA/2) recombinant inbred strains of mice to the Mls gene on chromosome one. To exclude the role of Ia antigens as the restricting determinants, monoclonal anti-Ia antibodies were used to block the in vitro proliferative response of this clone. Although anti-Iab and anti-Iad blocked the proliferation of this clone to KLH in the presence of irradiated spleen cells from either parent, this effect was shown to be dependent on Ia molecules passively absorbed by the T cell clone from the irradiated filler cells. Since the T clone expressed Thy-1.2 and Lyt-1+ differentiation markers, its helper activity was compared with other KLH carrier-specific clones in an in vitro antibody synthesis assay. The Mls-KLH-restricted T cell clone, in contrast to other carrier-specific, major histocompatibility complex (MHC)-restricted T cell clones, was unable to cooperate with trinitrophenyl (TNP)-primed B cells in the presence of TNP-KLH to generate an anti-TNP response. These experiments suggest that non-MHC determinants, such as autologous Mls gene products, may play a role in genetically restricted antigen recognition by T lymphocytes.	Waters SJ, Waksal SD, Norton GP, Bona CA	Antigen recognition by a t cell clone outside the context of the major histocompatibility complex	J Exp Med	159(1)	305-312	Jan	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6198425&dopt=Abstract	6198425 		04	6-8 wks	42	56	MF		cpm 	10955	777			11742	1564	781	1263			7541	786	378	126					10521	1445																					150	72							421	55																													6/30/2003	MK Sullivan	MK Sullivan										6198425.04
Total serum thyroxine (T4) content [µg/100ml]		We previously proposed that the audiogenic seizure (AGS) susceptibility of 21 +/- 1-day-old DBA/2 (D2) mice may result from an early postnatal elevation in serum thyroxine (T4) concentration. In the present study we used seven C57 X DBA (BXD) recombinant inbred strains and the D2.B6-Iasb congenic strain to study the association between serum T4 content and susceptibility to AGS. The D2.B6-Iasb congenic mice are genetically similar to the D2 mice except for the Iasb gene, which inhibits AGS susceptibility. The total and estimated free serum T4 concentrations in these strains at 14 +/- 1 days of age were compared with the previously determined AGS susceptibilities of these strains at 21 +/- 1 days of age. We found no significant correlations between serum T4 concentration and AGS susceptibility in these strains. It is unlikely, therefore, that inherited differences in neonatal serum T4 content are directly responsible for differences in susceptibility to AGS in 21 +/- 1-day-old mice. The mechanisms by which the experimental manipulation of serum T4 content influences AGS susceptibility are discussed.	Seyfried TN, Glaser GH, Yu RK	Genetic analysis of serum thyroxine content and audiogenic seizures in recombinant inbred and congenic strains of mice	Exp Neurol	83(2)	423-428	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6363115&dopt=Abstract	6363115 		01	13-15 days	13	15	MF	2-5	µg/100ml	6.7	0.5	10.3	1.1			10.2				6.0				6.2				8.6								8.7				7.3																		9.9																														6/30/2003	MK Sullivan	MK Sullivan										6363115.01
Estimated free serum thyroxine (T4) content [µg/100ml]		We previously proposed that the audiogenic seizure (AGS) susceptibility of 21 +/- 1-day-old DBA/2 (D2) mice may result from an early postnatal elevation in serum thyroxine (T4) concentration. In the present study we used seven C57 X DBA (BXD) recombinant inbred strains and the D2.B6-Iasb congenic strain to study the association between serum T4 content and susceptibility to AGS. The D2.B6-Iasb congenic mice are genetically similar to the D2 mice except for the Iasb gene, which inhibits AGS susceptibility. The total and estimated free serum T4 concentrations in these strains at 14 +/- 1 days of age were compared with the previously determined AGS susceptibilities of these strains at 21 +/- 1 days of age. We found no significant correlations between serum T4 concentration and AGS susceptibility in these strains. It is unlikely, therefore, that inherited differences in neonatal serum T4 content are directly responsible for differences in susceptibility to AGS in 21 +/- 1-day-old mice. The mechanisms by which the experimental manipulation of serum T4 content influences AGS susceptibility are discussed.	Seyfried TN, Glaser GH, Yu RK	Genetic analysis of serum thyroxine content and audiogenic seizures in recombinant inbred and congenic strains of mice	Exp Neurol	83(2)	423-428	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6363115&dopt=Abstract	6363115 		02	13-15 days	13	15	MF	2-5	µg/100ml	2.2	0.2	3.2	0.2			2.4				2.1				1.6				3.0								2.5				2.6																		3.4																														6/30/2003	MK Sullivan	MK Sullivan										6363115.02
Mean seizure severity [severity of seizure]		We previously proposed that the audiogenic seizure (AGS) susceptibility of 21 +/- 1-day-old DBA/2 (D2) mice may result from an early postnatal elevation in serum thyroxine (T4) concentration. In the present study we used seven C57 X DBA (BXD) recombinant inbred strains and the D2.B6-Iasb congenic strain to study the association between serum T4 content and susceptibility to AGS. The D2.B6-Iasb congenic mice are genetically similar to the D2 mice except for the Iasb gene, which inhibits AGS susceptibility. The total and estimated free serum T4 concentrations in these strains at 14 +/- 1 days of age were compared with the previously determined AGS susceptibilities of these strains at 21 +/- 1 days of age. We found no significant correlations between serum T4 concentration and AGS susceptibility in these strains. It is unlikely, therefore, that inherited differences in neonatal serum T4 content are directly responsible for differences in susceptibility to AGS in 21 +/- 1-day-old mice. The mechanisms by which the experimental manipulation of serum T4 content influences AGS susceptibility are discussed.	Seyfried TN, Glaser GH, Yu RK	Genetic analysis of serum thyroxine content and audiogenic seizures in recombinant inbred and congenic strains of mice	Exp Neurol	83(2)	423-428	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6363115&dopt=Abstract	6363115 		03	20-22 days	20	22	MF	2-5	Severity of seizure; 0=no response, 1=wild running, 2=clonic or tonic seizure	0.07		1.89				1.92				0.14				1.85				0.30								0.21				0.73																		0.09																														6/30/2003	MK Sullivan	MK Sullivan										6363115.03
Percent clonic tonic seizure [%]		We previously proposed that the audiogenic seizure (AGS) susceptibility of 21 +/- 1-day-old DBA/2 (D2) mice may result from an early postnatal elevation in serum thyroxine (T4) concentration. In the present study we used seven C57 X DBA (BXD) recombinant inbred strains and the D2.B6-Iasb congenic strain to study the association between serum T4 content and susceptibility to AGS. The D2.B6-Iasb congenic mice are genetically similar to the D2 mice except for the Iasb gene, which inhibits AGS susceptibility. The total and estimated free serum T4 concentrations in these strains at 14 +/- 1 days of age were compared with the previously determined AGS susceptibilities of these strains at 21 +/- 1 days of age. We found no significant correlations between serum T4 concentration and AGS susceptibility in these strains. It is unlikely, therefore, that inherited differences in neonatal serum T4 content are directly responsible for differences in susceptibility to AGS in 21 +/- 1-day-old mice. The mechanisms by which the experimental manipulation of serum T4 content influences AGS susceptibility are discussed.	Seyfried TN, Glaser GH, Yu RK	Genetic analysis of serum thyroxine content and audiogenic seizures in recombinant inbred and congenic strains of mice	Exp Neurol	83(2)	423-428	Feb	1984		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6363115&dopt=Abstract	6363115 		04	20-22 days	20	22	MF	2-5	%	1.8		91.4				92.0				0.0				93.0				0.0								0.0				35.0																		0.0																														6/30/2003	MK Sullivan	MK Sullivan										6363115.04
D-amphetamine-induced core temperature change [degrees C]		Two inbred strains of mice, DBA/2 and C57BL/6, differ in their responses to d-amphetamine-induced alteration of core temperature. At low doses of amphetamine (e.g., 2 mg/kg IP), both strains become markedly hypothermic within 10-20 minutes. High doses (e.g., 20 mg/kg IP) induce significant hyperthermia (+1.8 degrees C) in DBA/2 mice but have only a slight hyperthermic effect (+0.2-0.3 degrees C) effect on C57BL/6 mice. The phenotype of the F1 hybrid strain derived by crossing C57BL/6 by DBA/2 is indistinguishable from its C57BL/6 parent at a dose of 20 mg/kg IP, i.e., reduced responsiveness to amphetamine-induced hyperthermia is dominant. Analysis of the thermoregulatory responses of recombinant inbred derivatives (lines BXD-9, 11, 15, 19, 20, 21, 23, 27, 28, 30) suggest that the relative responses to amphetamine-induced hyperthermia is inherited in a simple Mendelian fashion. These results differ from other pairs of inbred mouse strains which have been compared. These findings identify yet another neuropharmacological difference between mouse strains C57BL/6 and DBA/2 and are reviewed in terms of neuroregulatory mechanisms effecting thermoregulation.	Seale TW, Carney JM, Johnson P, Rennert OM 	Inheritance of amphetamine-induced thermoregulatory responses in in bred mice	Pharmacol Biochem Behav	23(3)	373-377	Sep 	1985		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4048232&dopt=Abstract	4048232 		01	8 wks 	56		Male 	6	degrees C	0.42	0.391	1.66	0.418											1.26	0.497		1.55	0.520						0.42	0.202					1.77	0.304	0.41	0.209	0.21	0.213			1.56	0.515					1.78	0.312	1.46	0.536			1.36	0.621																											6/30/2003	MK Sullivan	MK Sullivan										4048232.01
Anti-F antigen (liver protein) titer, experiment 1 [log10 of the reciprocal of the dilution of serum required to bind 50% of the labeled antigen]		The immune response to the liver protein F antigen which, in the mouse, occurs in two allelic forms, is under sharp immunogenetic control in that only mice that possess the Ak molecule can respond to allo-F antigen. This response has been studied in a number of F1 hybrids between inbred strains and with recombinant inbred lines all of which express Ak, and which thus enable immune suppression effects to be detected. In the AKXL and AKXD sets the hybrids with CBA are responders if H-2k/H-2k, and usually nonresponders if H-2k/H-2b or H-2k/H-2d. Although this may be due to gene dosage effects, this cannot be the explanation for the low responsiveness of the H-2k/H-2b relative to the H-2k/H-2d mice found in CBA x BXD hybrids. For this, and other reasons, it seems likely that low responsiveness in any mouse possessing a responder Ak allele is due to suppression, and that this is mediated by the immune suppression effects of the non-H-2k haplotype. These H-2-mediated effects can be modified, both positively and negatively, by background genes. Thus, of the ten H-2k/H-2d members of the CBA x AKXD cross, seven are low responders and three are high responders. No other typed marker has the same strain distribution pattern at present. Major unresolved questions, therefore, concern the location and mechanism of action of the background genes and the mechanism of action of the H-2 immune suppression genes.	Oliveira DB, Nardi NB 	Immune suppression genes contol the anti-F antigen response in F1 hybrids and recombinant inbred sets of mice	Immunogenetics	26(6)	359-365		1987		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3117681&dopt=Abstract	3117681		01				MF	4-12	log10 of the reciprocal of the dilution of serum required to bind 50% of the labeled antigen							0.83	0.500	2.40	0.224			1.27	0.232					3.25	0.257							3.49	0.239	2.96	0.424							3.40	0.373			3.39	0.297	3.21	0.320																																			7/3/2003	MK Sullivan	MK Sullivan										3117681.01
Anti-F antigen (liver protein) titer, experiment 2		The immune response to the liver protein F antigen which, in the mouse, occurs in two allelic forms, is under sharp immunogenetic control in that only mice that possess the Ak molecule can respond to allo-F antigen. This response has been studied in a number of F1 hybrids between inbred strains and with recombinant inbred lines all of which express Ak, and which thus enable immune suppression effects to be detected. In the AKXL and AKXD sets the hybrids with CBA are responders if H-2k/H-2k, and usually nonresponders if H-2k/H-2b or H-2k/H-2d. Although this may be due to gene dosage effects, this cannot be the explanation for the low responsiveness of the H-2k/H-2b relative to the H-2k/H-2d mice found in CBA x BXD hybrids. For this, and other reasons, it seems likely that low responsiveness in any mouse possessing a responder Ak allele is due to suppression, and that this is mediated by the immune suppression effects of the non-H-2k haplotype. These H-2-mediated effects can be modified, both positively and negatively, by background genes. Thus, of the ten H-2k/H-2d members of the CBA x AKXD cross, seven are low responders and three are high responders. No other typed marker has the same strain distribution pattern at present. Major unresolved questions, therefore, concern the location and mechanism of action of the background genes and the mechanism of action of the H-2 immune suppression genes.	Oliveira DB, Nardi NB	Immune suppression genes contol the anti-F antigen response in F1 hybrids and recombinant inbred sets of mice	Immunogenetics	26(6)	359-365		1987		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3117681&dopt=Abstract	3117681		02				MF	6-12	log10 of the reciprocal of the dilution of serum required to bind 50% of the labeled antigen							1.07	0.331					1.03	0.563			2.36	0.312	1.76	0.518	1.65	0.511					1.81	0.493	1.92	0.503	0.76	0.500					2.41	0.225			2.11	0.402	2.31	0.321							2.39	0.321																											7/3/2003	MK Sullivan	MK Sullivan										3117681.02
Growth of syngeneic breast cancer tumors day 5 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		05	12 months	365		Female	5	mm3	20.6		33.3		18.9				14.7						40.2		27.5		38.7								33.7								22.7						52.6		32.0		37.4		58.7				47.1		57.2		25.8																								7/1/2003	MK Sullivan	MK Sullivan										12209979.05
Growth of syngeneic breast cancer tumors day 10 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		06	12 months	365		Female	5	mm3	42.5		35.0		34.1				41.3						54.3		45.3		73.1								44.7								40.7						119.6		84.2		53.2		106.0				87.3		131.1		50.4																								7/1/2003	MK Sullivan	MK Sullivan										12209979.06
Growth of syngeneic breast cancer tumors day 15 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		07	12 months	365		Female	5	mm3	89.3		70.8		72.2				81.4						73.4		67.0		96.3								76.2								83.0						157.5		164.7		78.1		187.9				185.0		201.3		75.2																								7/1/2003	MK Sullivan	MK Sullivan										12209979.07
Growth of syngeneic breast cancer tumors day 20 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		08	12 months	365		Female	5	mm3	41.4		106.3		52.8				43.2						139.3		112.5		149.7								119.6								52.2						279.2		263.1		170.0		198.3				266.7		279.2		127.0																								7/1/2003	MK Sullivan	MK Sullivan										12209979.08
Growth of syngeneic breast cancer tumors day 25 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		09	12 months	365		Female	5	mm3	17.2		187.0		35.1				37.3						177.9		162.6		189.3								179.2								15.8						283.3		279.0		214.7		326.0				355.0		328.1		182.5																								7/1/2003	MK Sullivan	MK Sullivan										12209979.09
Growth of syngeneic breast cancer tumors day 30 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		10	12 months	365		Female	5	mm3			212.9		14.4				19.2						224.9		188.3		252.3								173.0														358.4		369.6		231.3		388.5				504.3		460.5		222.0																								7/1/2003	MK Sullivan	MK Sullivan										12209979.1
Growth of syngeneic breast cancer tumors day 35 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		11	12 months	365		Female	5	mm3			254.2												185.1		275.8		301.7								279.2														502.6		468.3		190.8		500.5				662.1		724.6		262.5																								7/1/2003	MK Sullivan	MK Sullivan										12209979.11
Growth of syngeneic breast cancer tumors day 40 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		12	12 months	365		Female	5	mm3			315.6												70.2		335.5		135.3								303.6																		112.6										329.1																								7/1/2003	MK Sullivan	MK Sullivan										12209979.12
Growth of syngeneic breast cancer tumors day 45 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		13	12 months	365		Female	5	mm3			530.0												31.9		457.0		42.8								417.2																		49.6										448.6																								7/1/2003	MK Sullivan	MK Sullivan										12209979.13
Growth of syngeneic breast cancer tumors day 50 [mm3]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		14	12 months	365		Female	5	mm3			672.5												1.3		537.1		14.3								504.3																		20.9										623.0																								7/1/2003	MK Sullivan	MK Sullivan										12209979.14
Saccharin intakes post-saline, pre-exposed to saccharin, group 0 g/kg, residual mean [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	18	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	-0.12	0.10	0.16	0.09	-0.22	0.14	0.54	0.30	0.14	0.20	-0.00	0.08	-0.13	0.09	0.26	0.18	-0.06	0.11	-0.22	0.15	-0.16	0.12	0.20	0.12	0.40	0.14	-0.16	0.08	-0.16	0.24					0.11	0.26					-0.18	0.16	-0.56	0.13	-0.17	0.16	0.06	0.12	-0.15	0.19					0.36	0.12																							7/2/2003	MK Sullivan	MK Sullivan										9756038.18
Ethanol induced conditioned taste aversion to saccharin, group 2 g/kg, residual mean [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	19	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.13	0.09	0.05	0.10	0.04	0.16	0.33	0.32	-0.71	0.20	-0.18	0.12	0.12	0.13	-0.09	0.24	-0.24	0.07	-0.16	0.14	0.29	0.24	0.00	0.15	0.38	0.12	0.18	0.14	0.17	0.18					0.01	0.18					-0.30	0.16	-0.64	0.13	-0.00	0.12	-0.13	0.19	0.22	0.13					0.15	0.15																							7/2/2003	MK Sullivan	MK Sullivan										9756038.19
Ethanol induced conditioned taste aversion to saccharin, group 4 g/kg, residual mean [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	20	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.24	0.04	-0.48	0.11	0.22	0.18	0.28	0.16	-0.91	0.17	0.09	0.16	0.26	0.05	-0.13	0.31	0.06	0.10	0.03	0.12	-0.18	0.18	0.06	0.19	-0.03	0.19	0.55	0.11	0.49	0.18					0.08	0.20					-0.33	0.17	-0.41	0.09	0.17	0.16	0.08	0.20	-0.22	0.19					-0.30	0.18																							7/2/2003	MK Sullivan	MK Sullivan										9756038.2
Saccharin intake post EtOH no saccharin pre-exposure, group UP, residual mean [ml]		Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced conditioned taste aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced conditioned taste aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, conditioned place preference). However, there were significant genetic correlations between taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that taste aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced conditioned taste aversion. Some of these genes appear to influence taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.	Risinger FO, Cunningham CL	Ethanol-induced conditioned taste aversion in BXD recombinant inbred mice	Alcohol Clin Exp Res	22(6)	1234-1244	Sept	1998		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9756038&dopt=Abstract	9756038	98427469	21	56-125 days	56	125	Male	2-14	ml saccharin intake/total fluid intake	0.10	0.08	0.46	0.14	-0.14	0.14	-0.01	0.46	-0.16	0.19	0.06	0.08	-0.39	0.16	0.19	0.24	0.01	0.20	-0.08	0.13	-0.26	0.19	-0.00	0.17	0.43	0.19	-0.09	0.11	-0.12	0.30					0.01	0.21					-0.08	0.17	-0.52	0.09	0.09	0.15	-0.17	0.23	0.30	0.12					-0.13	0.17																							7/2/2003	MK Sullivan	MK Sullivan										9756038.21
Tyrosine hydroxylase neurons in ventral tegmental area [average cell number/section]		BACKGROUND It has not been established to what extent the natural variation in dopamine systems contribute to the variation in ethanol response. The current study addresses this issue by measuring D dopamine (DA) receptor binding, the expression of, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of ethanol and other drug-related phenotypes.(2)METHODS Data were collected for 21 to 23 of the BXD RI strains and the parental strains. D DA receptor autoradiography was performed using I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025]. expression was measured using the Affymetrix oligoarray system. Immunocytochemical techniques were used to determine the number of midbrain DA neurons [Hitzemann B, Dains K, Hitzemann R (1994) Further studies on the relationship between dopamine cell density and haloperidol response. J Pharmacol Exp Ther 271:969-976].(2)RESULTS AND CONCLUSIONS The range of difference in receptor binding for the RI strains was approximately 2-fold in all regions examined, the core, the shell of the nucleus accumbens (NAc) and the dorsomedial caudate-putamen (CPu); heritability in all regions was moderate-( 2 approximately 0.35). expression in forebrain samples from the RI and parental strains ranged 1.5- to 2-fold and was moderate-0.47. Variation in the number of tyrosine hydroxylase (TH) positive neurons was moderate, 41% and 26% and was low-0.19 and 0.15 for the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Significant correlations were found between D DA receptor binding and the low dose (1.33 g/kg) ethanol stimulant response. ( < 0.002) and between expression and conditioned place preference (CPP) ( < 0.0005). No significant correlations were detected between ethanol preference and either receptor binding or expression; however, a significant correlation was found between preference and expression. is approximately 0.2 Mb from. Overall, the data suggest ethanol preference and CPP are associated with the expression of or closely linked genetic loci.(2)	Hitzemann R, Hitzemann B,  Rivera S, Gatley J, Thanos P, Siming Shou LL, Williams RW	Dopamine D2 receptor binding, Drd2 Expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to alcohol and other drug associated phenotypes	Alcohol Clin Exp Res	27(1)	1-11	Jan	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12543998&dopt=Abstract	12543998		04				Male	10-15	average cell number/section	94	2.4	110	2.4	78	1.5	93	1.8	93	3.4	94	1.9	95	2.0	81	1.9	91	1.5	89	1.6	98	1.5	92	1.8	92	2.2	102	1.9	105	3.6	101	1.7	89	2.3	86	1.4	91	2.0	93	3.7	100	2.3	99	1.6	74	3.2	85	1.6	86	1.8	78	0.6	82	1.8	78	1.6																							7/2/2003	MK Sullivan	MK Sullivan										12543998.04
Tyrosine hydroxylase neurons in substantia nigra compacta [average cell number/section]		BACKGROUND It has not been established to what extent the natural variation in dopamine systems contribute to the variation in ethanol response. The current study addresses this issue by measuring D dopamine (DA) receptor binding, the expression of, the number of midbrain DA neurons in the BXD recombinant inbred (RI) series and then compares these strain means with those previously reported for a variety of ethanol and other drug-related phenotypes.(2)METHODS Data were collected for 21 to 23 of the BXD RI strains and the parental strains. D DA receptor autoradiography was performed using I-epidepride as the ligand [ Kanes S, Dains K, Cipp L, Gatley J, Hitzemann B, Rasmussen E, Sanderson S, Silverman S, Hitzemann R (1996) Mapping the genes for haloperidol-induced catalepsy. J Pharmacol Exp Ther 277:1016-1025]. expression was measured using the Affymetrix oligoarray system. Immunocytochemical techniques were used to determine the number of midbrain DA neurons [Hitzemann B, Dains K, Hitzemann R (1994) Further studies on the relationship between dopamine cell density and haloperidol response. J Pharmacol Exp Ther 271:969-976].(2)RESULTS AND CONCLUSIONS The range of difference in receptor binding for the RI strains was approximately 2-fold in all regions examined, the core, the shell of the nucleus accumbens (NAc) and the dorsomedial caudate-putamen (CPu); heritability in all regions was moderate-( 2 approximately 0.35). expression in forebrain samples from the RI and parental strains ranged 1.5- to 2-fold and was moderate-0.47. Variation in the number of tyrosine hydroxylase (TH) positive neurons was moderate, 41% and 26% and was low-0.19 and 0.15 for the ventral tegmental area (VTA) and substantia nigra compacta (SNc), respectively. Significant correlations were found between D DA receptor binding and the low dose (1.33 g/kg) ethanol stimulant response. ( < 0.002) and between expression and conditioned place preference (CPP) ( < 0.0005). No significant correlations were detected between ethanol preference and either receptor binding or expression; however, a significant correlation was found between preference and expression. is approximately 0.2 Mb from. Overall, the data suggest ethanol preference and CPP are associated with the expression of or closely linked genetic loci.(2)	Hitzemann R, Hitzemann B,  Rivera S, Gatley J, Thanos P, Siming Shou LL, Williams RW	Dopamine D2 receptor binding, Drd2 Expression and the number of dopamine neurons in the BXD recombinant inbred series: genetic relationships to alcohol and other drug associated phenotypes	Alcohol Clin Exp Res	27(1)	1-11	Jan	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12543998&dopt=Abstract	12543998		05				Male	10-15	average cell number/section	142	2.0	173	2.4	125	2.5	132	2.3	117	5.3	135	1.8	124	3.0	129	1.8	136	1.5	127	1.5	140	1.7	148	2.1	141	1.7	142	1.7	147	3.3	142	1.9	135	2.0	136	2.2	142	2.0	136	2.2	136	2.1	130	2.2	129	2.8	132	2.1	127	1.5	118	1.92	129	2.0	118	2.5																							7/2/2003	MK Sullivan	MK Sullivan										12543998.05
BEC after ethanol injection, 1.5 g/kg (raises BEC to ~1.5 mg EtOH/ml blood and then stabilize with daily pyrazole injections), mg/ml		Male mice from C57BL/6J (B6), DBA/2J (D2) and their 25 recombinant inbred (RI) strains were exposed to ethanol (EtOH) vapor (3.0-9.0 mg EtOH/liter of air) for 72 hr. Mice were selected such that each strain averaged 1.34 to 1.59 mg of EtOH/ml of blood on withdrawal. Control groups and EtOH-exposed groups were tested hourly for handling-induced convulsions (HIC) for 10 hr and at hr 24 and 25. Strain withdrawal severity was indexed as the area under the 25-hr HIC curve for the EtOH group minus that strain's equivalent value for the control group. Genome-wide quantitative trait locus (QTL) analyses correlating strain means with allelic status at > 1500 markers identified 10 chromosomal regions at P < .01. These provisionally identified QTLs were on chromosomes 1 (2 QTLs), 3, 9 (2 QTLs), 10, 12, 13, 15 and 18. Multiple regression analysis using the four most influential QTLs revealed that these loci controlled 86% of the genetic variance. A QTL mapped to distal chromosome 1 (P < .001) is in the same region as one previously definitively mapped for acute alcohol withdrawal, as well as one mapped for acute pentobarbital withdrawal. Several of the QTLs map near potential candidate genes. These provisional linkages will now be confirmed or rejected using additional genetically segregating populations.	Crabbe JC 	Provisional mapping of quantitative trait loci for chronic ethanol withdrawal severity in BXD recombinant inbred mice	J Pharmacol Exp Ther	286(1)	263-271	Jul	1998 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9655868&dopt=Abstract	9655868		04				Male	3-52	mg/ml	1.51	0.09	1.50	0.06	1.51	0.18	1.53	0.11	1.48	0.21	1.47	0.14	1.49	0.14	1.52	0.15	1.50	0.12	1.51	0.07	1.54	0.13	1.50	0.11	1.53	0.16	1.49	0.10	1.49	0.13	1.49	0.10			1.50	0.09	1.48	0.09	1.34	0.60	1.49	0.09	1.59	0.34	1.51	0.12	1.50	0.19	1.49	0.08	1.54	0.12	1.51	0.09	1.51	0.09																							7/2/2003	MK Sullivan	MK Sullivan										9655868.04
Mean audiogenic seizure severity  [severity of seizure] 		Mice of some inbred strains, such as 21-day-old DBA/2J mice, have generalized convulsions when exposed to intense auditory stimulation. Analysis of susceptibility to audiogenic seizures in BXD recombinant inbred strains has demonstrated the influence of at least three loci. One locus, Asp-1, is located on chromosome 12 between Ah and D12Nyu1; another locus, Asp-2, is on chromosome 4, tightly linked to b. Here we report evidence that Asp-2 is located within an 8-centimorgan segment distal to b and that Asp-3 is linked to Mtv-1 on chromosome 7. We also present evidence that these three loci account for most of the heritable variation in susceptibility to audiogenic seizures in crosses of DBA/2J and C57BL/6J mice and that susceptibility to audiogenic seizures is influenced by genomic imprinting. Thus, genomic imprinting may complicate linkage and mapping studies and should be considered in analyses of complex modes of inheritance.	Neumann PE, Collins RL	Genetic dissection of susceptibility to audiogenic seizures in inbred mice.	Proc Natl Acad Sci	88(12)	5408-5412	Jun 	1991 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2052619&dopt=Abstract	2052619		02 	21 days	21		MF		Severity of seizure; 0=no response, 1=wild running, 2=clonic or tonic seizure	0.07		1.88		0.20		1.92		1.64		0.14		0.57		1.85		1.04		0.30		0.10		0.33		1.94		0.21		0.07		0.73				1.92				1.16		1.09		0.36		1.29		1.00		0.09		0.00				1.90																								7/1/2003	MK Sullivan	MK Sullivan										2052619.02
Tolerance or sensitization to ethanol effects on locomotor activity - Difference between experimental group (two prior exposures to 2g/kg ip EtOH) and saline control group, 4th conditioning day [activity counts/min]		Genetic differences in ethanol's ability to induce conditioned place preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor preference testing without ethanol revealed significant genetic differences in conditioned place preference, with some strains spending nearly 80% time on the ethanol-paired floor while others spent only 50% (i.e., no preference). Control mice showed genetic differences in unconditioned preference for the floor cues, but unconditioned preference was not genetically correlated with conditioned preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of conditioned place preference. However, there was a significant negative genetic correlation (r = -0.42) between test session activity and preference. Quantitative trait loci (QTL) analyses showed strong associations (P < 0.01) between conditioned place preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01 < P < 0.05) were identified on several other chromosomes. Analysis also yielded several significant QTL for unconditioned preference, ethanol-stimulated activity, and sensitization. Overall, these data support the conclusion that genotype influences ethanol-induced conditioned place preference, presumably via genetic differences in sensitivity to ethanol's rewarding effects. Moreover, several chromosomal regions containing candidate genes of potential relevance to ethanol-induced conditioned place preference have been identified.	Cunningham CL 	Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice	Psychopharmacology	120(1)	28-41	July	1995 		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7480533&dopt=Abstract	7480533	96078685	17	56-125 days	56	125	Male	13-34	activity counts/min	17.954	3.97	112.444	7.61	36.212	8.40	30.788	4.90	27.695	3.25	10.331	2.50	94.338	10.07	85.444	6.48	37.384	6.78	11.907	3.66	46.397	6.39	52.106	6.28	11.656	3.10	3.311	2.87	57.404	6.93					67.040	7.54	41.583	3.86			41.868	5.29	66.298	9.60	99.001	12.7	21.788	5.10	46.616	7.63																													7/3/2003	MK Sullivan	MK Sullivan										7480533.17
Leukocyte infiltration in metastatic breast tumor, day 5 [measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		15	12 months	365		Female	5	Measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe	2.07	0.156	0.91	0.113	2.52	0.498			2.64	0.406					0.49	0.505	0.25	0.251									1.51	0.502							1.92	0.108																			0.99	0.079																							6/30/2003	MK Sullivan	MK Sullivan										12209979.15
Leukocyte infiltration in metastatic breast tumor, day 12 [measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		16	12 months	365		Female	5	Measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe	3.63	0.101	0.81	0.207	3.34	0.294			3.28	0.054					2.73	0.297	1.00	0.498	1.97	0.149							0.78	0.242							3.32	0.397					0.30	0.108			1.82	0.197							0.62	0.092	1.07	0.152																							6/30/2003	MK Sullivan	MK Sullivan										12209979.16
Leukocyte infiltration in metastatic breast tumor, day 30 [measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		17	12 months	365		Female	5	Measured on scale of 0=no leukocyte infiltration and no destruction of implanted tumor cell to 4=most severe	2.12	0.117			2.37	0.162			2.71	0.197					3.55	0.100			3.34	0.210															2.84	0.194									3.39	0.340									0.50	0.491																							6/30/2003	MK Sullivan	MK Sullivan										12209979.17
T cell infiltration at tumor site in breast cancer cells, day 5 [measured on scale of 0=no T-cell infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		18	12 months	365		Female	5	Measured on scale of 0=no T cell infiltration and no destruction of implanted tumor cell to 4=most severe	0.86	0.062			2.02	0.210			1.93	0.288																									1.66	0.155																																											6/30/2003	MK Sullivan	MK Sullivan										12209979.18
T cell infiltration at tumor site in breast cancer cells, day 1 [measured on scale of 0=no T-cell infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		19	12 months	365		Female	5	Measured on scale of 0=no T cell infiltration and no destruction of implanted tumor cell to 4=most severe	3.64	0.116	1.13	0.098	3.33	0.295			3.28	0.051					1.72	0.295	1.52	0.000	1.46	0.348							1.27	0.239							3.85	0.102									1.82	0.207							0.47	0.068	1.07	0.157																							6/30/2003	MK Sullivan	MK Sullivan										12209979.19
T cell infiltration at tumor site in breast cancer cells, day 30 [measured on scale of 0=no T-cell infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		20	12 months	365		Female	5	Measured on scale of 0=no T cell infiltration and no destruction of implanted tumor cell to 4=most severe	1.62	0.594			2.37	0.166			2.73	0.192					3.52	0.106	0.18	0.046	3.69	0.160							0.29	0.114							2.34	0.307									3.38	0.364									0.24	0.000																							6/30/2003	Mk Sullivan	MK Sullivan										12209979.2
Apoptosis of breast tumor cells, day 12 [measured on scale of 0=no apoptosis infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		21	12 months	365		Female	5	Measured on scale of 0=no apoptosis infiltration and no destruction of implanted tumor cell to 4=most severe	3.50	0.302	0.30	0.108	3.31	0.289			3.26	0.050					0.10	0.166	0.82	0.102	0.83	0.042							0.61	0.203							3.37	0.347									1.09	0.219									0.70	0.206																							6/30/2003	MK Sullivan	MK Sullivan										12209979.21
Apoptosis of breast tumor cells, day 30 [measured on scale of 0=no apoptosis infiltration and no destruction of implanted tumor cell to 4=most severe]		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		22	12 months	365		Female	5	Measured on scale of 0=no apoptosis infiltration and no destruction of implanted tumor cell to 4=most severe	1.11	0.102			2.35	0.148			2.21	0.277					2.85	0.105	0.46	0.037	2.40	0.081															1.81	0.206									3.09	0.00									0.30	0.308																							6/30/2003	MK Sullivan	MK Sullivan										12209979.22
Mixed lymphocyte reaction (MLR) with BALB/c spleen cells [cpm stimulated/cpm unstimulated] 		To develop a better animal model for studying the effects of the host environment in neoplasia, we injected various genetically well-characterized H-2(d) RI strains of BXD mice with syngeneic breast cancer cells (TS/A) and monitored the growth of tumors over time. There was a marked difference in the growth of the implanted breast cancer cells among the 14 BXD RI strains, with 4 patterns of tumor development being observed: in type I, the implanted tumor cells grew rapidly in the first 2 weeks, necrosis of the tumors was observed and metastases to the intestinal lymph nodes and pancreas was observed, causing death; in type II, the implanted tumor cells grew slowly and attained a size after day 50 that required killing the animal, with tumor necrosis being rare and metastases absent; in type III, the implanted tumor cells grew initially but underwent a slow decline after 4 weeks; and in type IV, the implanted tumor cells failed to develop. Apoptosis of the implanted tumor cells was responsible for the regression of tumor nodules. The T-cell immune response minimized tumor development in types III and IV since T-cell depletion of the BXD RI mice resulted in aggressively growing tumors in these strains. 	Grizzle WE, Mountz JD, Yang PA, Xu X, Sun S, Van Zant GE, Williams RW, Hsu HC, Zhang HG.	BXD recombinant inbred mice represent a novel T cell-mediated immune response tumor model.	Int J Cancer 	101(3)	270-279	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12209979&dopt=Abstract	12209979 		23	12 months	365		Female	5	cpm stimulated/cpm unstimulated 					1.59	0.395			1.79	0.329			55.00	11.272	1.33	0.316	1.40	0.285	1.67	3.73											43.62	8.048			2.44	0.474									2.25	0.307					7.72	1.368																											6/30/2003	MK Sullivan	MK Sullivan										12209979.23
Brain to Body ratio		Adult C57BL/6J (B6) male mice had 37% heavier brains than did DBA/2J (D2) mice, while their body weights did not differ. The BXD recombinant inbred (RI) series of 20 strains, derived from a cross between B6 and D2 inbred strains, was used as the initial screen to determine significant associations between male brain weight and brain:body weight ratio, with allelic variation at 360 known marker gene loci. For brain weight, this yielded five candidate chromosome regions, each reflecting a possible quantitative trait locus (QTL) site affecting brain weight. The second step was to test as many of these five as possible using standard (non-RI) inbred strain data for brain weight previously reported in the literature. For this purpose, only strains possessing the same alleles as the B6 or D2 strains were used. Sufficient data to test two of the five candidate QTL were available. Of these, one was strongly supported as a site affecting brain weight--the D7rp2 region of chromosome 7. For the brain to body weight ratio, four chromosome regions emerged as significantly associated in the BXD series, but none were amenable to testing due to a lack of allelic information for the standard inbred strains. However, two of these regions showed highly significant associations (p less than 0.001, single test) that merit consideration as QTL sites for future testing. These two are the Hba region on chromosome 11 and the D17Tu7 region on chromosome 17. The genetic correlation between brain and body weight was low (r = 0.28), indicating that these two traits are largely genetically independent in the BXD RI series.	Belknap JK, Phillips TJ, O'Toole LA.	Quantitative trait loci associated with brain weight in the BXD/Ty recombinant inbred mouse strains	Brain Res Bul 	29(3-4)	337-344	Sept-Oct	1992		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1393606&dopt=Abstract	1393606		03	11-13 wks	77	91	Male	7-8		0.0183	0.0014	0.0134	0.0016	0.0163	0.0011	0.0138	0.0012	0.0183	0.0011	0.145	0.0007	0.0160	0.0006	0.0154	0.0010			0.0164	0.0006	0.0138	0.0011	0.0145	0.0006	0.0155	0.0008	0.0163	0.0009	0.0149	0.0009					0.0145	0.0016	0.0172	0.0004	0.0179	0.0017	0.0153	0.0010	0.0161	0.0016	0.0152	0.0012	0.0148	0.0011	0.0153	0.0015																													7/7/2003	MK Sullivan	MK Sullivan										1393606.03
B-mannosidase activity in liver of Female [mg p-nitrophenl liberated/g tissue wet weight/hr at 37 degrees C]		A gene (Bmn) with a major effect on beta-mannosidase activity in kidney and liver of the house mouse was revealed by assay with the synthetic substrate p-nitrophenyl-beta-D-mannoside. Activity is low in DBA/2J and CSB mice and high in C57BL/6J mice. By the use of the BXD series of recombinant inbred strains and by crosses between C57BL and CSB, it was possible to map the gene to the distal part of chromosome 3 by demonstration of linkage to a gene for cadmium resistance, cdm, as well as to the Adh-3 locus.	Lundin LG	A gene (Bmn) controlling B-mannosidase activity in the mouse is located in the distal part of chromosome 3	Biochem Genet 	25(7-8)	603-610 	Aug	1987 		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3447593&dopt=Abstract	3447593		01				Female		mg p-nitrophenl liberated/g tissue wet weight/hr at 37 degrees C	2.187		1.734		1.676		1.536		2.741		1.633		1.051		1.813		1.439		1.466				1.956		2.548		2.717		1.524		1.460				1.608		1.829				1.658		1.732		2.529		1.636		2.567				2.275		1.304																								7/8/2003	MK Sullivan	MK Sullivan										3447593.01
Seizure threshold pressure at compression rate of 100 atm hr-1 (100iPc) [atm]		Most mammals tested, when exposed to increasing pressure in helium/oxygen atmospheres, exhibit progressive motor disturbances culminating in two, usually successive, well-differentiated convulsive seizures. The seizures are highly reproducible components of the constellation of events that collectively constitute the High Pressure Neurologic Syndrome (HPNS). In the present study, we present evidence that the mean difference in seizure threshold pressures of the first seizure to occur (HPNS Type I) between inbred mouse strains DBA/2J and C57BL/6J is predominantly determined (greater than 60%) by the expression of a major locus-possibly linked to the H-2 locus on chromosome 17- and a minor locus, probably unlinked. This outcome is derived from applications of the maximum likelihood modeling procedure of ELSTON and STEWART (1973) and STEWART and ELSTON (1973) to eleven models of genetic determinacy and tests (including breeding tests) of "preferred" models so derived using BXD recombinant inbred strains that show the following: The major locus exhibits conditional dominance characteristics depending upon compression rate and minor locus genotype. At a constant mean compression rate of 100 atm hr-1, the major locus manifests strong, though incomplete, dominance apparently independent of minor locus genotype. Its expression is, however, highly sensitive to compression rate, losing its dominance altogether at a linear rate of 1,000 atm hr-1. The major locus interacts with the weakly dominant and relatively compression-rate-insensitive minor locus to retain dominance at fast compression only when the dominant alleles of both loci are present. A principal finding of this study is that employing two compression rates permits fuller genetic characterization of murine high-pressure seizure susceptibility differences than could be achieved by use of a single compression rate.	McCall RD, Frierson D Jr.	Evidence that two loci predominantly determine the difference in susceptibility to the high pressure neurologic syndrome type 1 seizure in mice	Genetics	99(2)	285-307	Oct 	1981		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7341354&dopt=Abstract	7341354 		01	35-80 days	35	80	MF		atm 	89.1		69.9		89.7		89.0		71.5				81.8		82.9		74.5		77.0				83.0		81.7		72.0		88.9		85.8		84.9		89.0				82.0		72.9		76.7		74.5		84.3		89.9		73.1																												7/8/2003	MK Sullivan	MK Sullivan										7341354.01
Seizure threshold pressure at compression rate of 1000 atm hr-1 (1000iPc) [atm]		Most mammals tested, when exposed to increasing pressure in helium/oxygen atmospheres, exhibit progressive motor disturbances culminating in two, usually successive, well-differentiated convulsive seizures. The seizures are highly reproducible components of the constellation of events that collectively constitute the High Pressure Neurologic Syndrome (HPNS). In the present study, we present evidence that the mean difference in seizure threshold pressures of the first seizure to occur (HPNS Type I) between inbred mouse strains DBA/2J and C57BL/6J is predominantly determined (greater than 60%) by the expression of a major locus-possibly linked to the H-2 locus on chromosome 17- and a minor locus, probably unlinked. This outcome is derived from applications of the maximum likelihood modeling procedure of ELSTON and STEWART (1973) and STEWART and ELSTON (1973) to eleven models of genetic determinacy and tests (including breeding tests) of "preferred" models so derived using BXD recombinant inbred strains that show the following: The major locus exhibits conditional dominance characteristics depending upon compression rate and minor locus genotype. At a constant mean compression rate of 100 atm hr-1, the major locus manifests strong, though incomplete, dominance apparently independent of minor locus genotype. Its expression is, however, highly sensitive to compression rate, losing its dominance altogether at a linear rate of 1,000 atm hr-1. The major locus interacts with the weakly dominant and relatively compression-rate-insensitive minor locus to retain dominance at fast compression only when the dominant alleles of both loci are present. A principal finding of this study is that employing two compression rates permits fuller genetic characterization of murine high-pressure seizure susceptibility differences than could be achieved by use of a single compression rate.	McCall RD, Frierson D Jr.	Evidence that two loci predominantly determine the difference in susceptibility to the high pressure neurologic syndrome type 1 seizure in mice	Genetics	99(2)	285-307	Oct 	1981		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7341354&dopt=Abstract	7341354 		02	35-80 days	35	80	MF		atm 	79.8		62.6		65.9		80.6		67.6				77.4		66.7		66.1		67.3				68.8		79.9		67.6		71.4		80.0		77.9		77.2				80.5		65.3		63.4		67.4		71.1		78.7		64.3																												7/8/2003	MK Sullivan	MK Sullivan										7341354.02
Mean water consumption, water offered vs. 10 % ethanol [ml]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		08	51-125 days	51	125	Female	10-18	ml	4.82	0.514	2.25	0.400			4.65	0.708	3.54	0.603	3.75	0.402			4.23	0.517			3.06	0.308	4.64	0.410	6.82	0.301	3.55	0.610	4.13	0.615	4.95	0.310	4.65	0.508			4.45	0.402			4.54	0.505	2.35	0.302	3.63	0.419	3.05	0.604			5.55	0.514			2.36	0.500	5.25	0.606																							7/11/2003	MK Sullivan	MK Sullivan										7978106.08
Mean water consumption, water offered vs. 0.2 % saccharin [ml]		The genomic map locations of specific genes controlling behaviors can be identified by studying a panel of recombinant inbred (RI) mouse strains. The progenitor C57BL/6J (B6) and DBA/2J (D2) strains, and 19 of the BXD RI strains derived from an F2 cross of these progenitors, were tested for 3% and 10% ethanol (EtOH) intake. The test sequence began with two-bottle free choice between tap water and unsweetened ethanol, and ended with free choice between water and saccharin-sweetened ethanol. Saccharin preference was also measured. Correlational analyses indicated that 59% of the genetic variance in 10% ethanol and sweetened 10% ethanol consumption was held in common, 24% of the genetic variance in saccharin and sweetened 10% ethanol consumption was held in common, and only 7% of the genetic variance in saccharin and unsweetened 10% ethanol consumption was held in common. These percentages for 3% ethanol solutions were 21%, 36%, and 14%. In addition, the severity of handling-induced convulsions during ethanol withdrawal was found to be significantly associated with the amount of ethanol consumed from the sweetened ethanol drinking tubes, suggesting that genetic differences in avidity for ethanol could lead to the development of physical dependence. Quantitative trait loci (QTL) analyses revealed that several genetic markers were associated with ethanol consumption levels, including markers for the D2 dopamine receptor. QTL analyses of saccharin and sweetened ethanol consumption identified the sac locus, thought to determine the ability to detect saccharin. In general, our results suggest that saccharin and ethanol consumption are determined by the actions of multiple genes (QTL), some in common, and suggest specific map locations of several such QTL on the mouse genome.	Phillips TJ, Crabbe JC, Metten P, Belknap JK.	Localization of genes affecting alcohol drinking in mice.	Alcohol Clin Exp Res	18(4)	931-941	Aug	1994		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7978106&dopt=Abstract	7978106		09	51-125 days	51	125	Female	10-18	ml	1.40	0.696	0.38	0.221			4.75	0.919	1.86	0.514	0.11	0.00			0.73	0.416			1.10	0.526	0.49	0.190	1.79	0.806	0.79	0.520	1.51	0.517	0.70	0.318	1.08	0.542			0.39	0.227			2.60	0.787	0.09	0.000	0.20	0.114	0.60	0.215			0.49	0.314			1.41	0.507	0.70	0.424																							7/11/2003	MK Sullivan	MK Sullivan										7978106.09
Total fluid intake during forced alcohol exposure period [mls/day]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		01	8 wks	56		MF	3-9	mls/day	5.23	0.226	4.96	0.257	6.39	0.327					4.65	0.226	6.07	0.142			4.38	0.161									5.39	0.368																			5.09	0.510							6.62	0.296																							7/11/2003	MK Sullivan	MK Sullivan										8651451.01
Total fluid intake during free choice alcohol  period [mls/day]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		02	8 wks	56		MF	3-9	mls/day	6.06	0.248	6.64	0.182	2.50	0.146					5.26	0.224	7.04	0.273			6.02	0.272									6.35	0.242																			5.89	0.330							7.19	0.14																							7/11/2003	MK Sullivan	MK Sullivan										8651451.02
Mean alcohol preference during free choice period for males [mls 10 % ethanol/mls total fluid]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		03	8 wks	56		Male	18-20	mls 10 % ethanol/mls total fluid	0.83	0.027	0.16	0.019	0.27	0.042					0.83                                                                                                     	0.026	0.24	0.068			0.43	0.106									0.79	0.073																			0.24	0.071							0.16	0.012																							7/11/2003	MK Sullivan	MK Sullivan										8651451.03
Mean alcohol preference during free choice period for females [mls 10 % ethanol/mls total fluid]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		04	8 wks	56		Female	18-20	mls 10 % ethanol/mls total fluid	0.81	0.030	0.14	0.011	0.48	0.063					0.71	0.046	0.46	0.083			0.29	0.105									0.63	0.064																			0.45	0.099							0.19	0.028																							7/11/2003	MK Sullivan	MK Sullivan										8651451.04
Mean alcohol consumption during free choice period for males [gms ethanol/kg body weight/day]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		05	8 wks	56		Male	18-20	gms ethanol/kg body weight/day	14.8	0.54	3.8	0.59	5.2	0.82					12.9	0.75	4.4	1.27			9.5	2.52									13.3	1.50																			4.5	1.16							7.0	0.69																							7/11/2003	MK Sullivan	MK Sullivan										8651451.05
Mean alcohol consumption during free choice period for females [gms ethanol/kg body weight/day]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		06	8 wks	56		Female	18-20	gms ethanol/kg body weight/day	20.5	1.44	3.7	0.48	12.2	1.76					17.5	1.68	9.1	2.00			7.2	2.18									17.1	1.84																			9.2	1.94							4.7	0.60																							7/11/2003	MK Sullivan	MK Sullivan										8651451.06
Mean body weight [g]                                                                                                                                                                                                                                                                                                            		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		07	8 wks	56		MF	18-20	g	23.5	0.79	22.9	0.46	22.6	0.79					21.4	0.68	23.9	0.60			20.5	0.65									23.5	0.79																			23.3	1.05							22.7	0.94																							7/11/2003	MK Sullivan	MK Sullivan										8651451.07
Alcohol preference ratio [mls 10 % ethanol/mls total fluid]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		08	8 wks	56		MF	18-20	mls 10 % ethanol/mls total fluid	0.82	0.02	0.15	0.01	0.35	0.04					0.76	0.03	0.38	0.05			0.37	0.07									23.5	0.79																			0.37	0.07							0.18	0.02																							7/11/2003	MK Sullivan	MK Sullivan										8651451.08
Alcohol consumption ratio [gms ethanol/kg body weight]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		09	8 wks	56		MF	18-20	gms ethanol/kg body weight	17.4	0.85	3.7	0.36	8.0	1.23					15.1	0.96	8.7	1.15			8.5	1.73									15.2	1.24																			7.4	1.45							5.1	0.63																							7/11/2003	MK Sullivan	MK Sullivan										8651451.09
Catalase activity in liver [µMol]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		10	8 wks	56		MF	15-18	µMol	68.4	3.9	115.9	5.9	71.1	4.6					76.2	4.3	0.0	0.0			130.9 	5.2									106.8	7.3																			121.6	7.3							136.0	6.0																							7/11/2003	MK Sullivan	MK Sullivan										8651451.1
Catalase activity in brain [nMol]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		11	8 wks	56		MF	15-18	nMol	517.0	31	750.1	68	785.8	25					627.3	31	0.0	0.0			660.0	34									636.7	43																			615.1	33							795.8	37																							7/11/2003	MK Sullivan	MK Sullivan										8651451.11
ALDH activity in liver [nMol NADH produced/minute/milligram of protein]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		12	8 wks	56		MF	15-18	nMol NADH produced/minute/milligram of protein	23.6	1.7	21.6	1.5	14.1	1.0					15.3	0.9	15.0	1.2			12.4	1.3									15.7	1.1																			21.3	3.3							13.6	1.1																							7/11/2003	MK Sullivan	MK Sullivan										8651451.12
ALDH activity in brain [nMol NADH produced/minute/milligram of protein]		Studies were initiated to characterize behaviorally and biochemically C57BL/6J and DBA/2J inbred mice, as well as BXD Recombinant Inbred (RI) strains derived from them. The C57BL/6J, DBA/2J, and 7 BXD RI strains were tested for voluntary alcohol consumption (VAC) by receiving 4 days of forced exposure to a 10% (w/v) solution of alcohol, followed by 3 weeks of free choice between water and 10% alcohol. Measures of VAC included the absolute intake of alcohol (g/kg), as well as alcohol preference. A wide range of VAC was displayed by the various BXD RI strains with a continuous (rather than bimodal) distribution, indicating that there is likely to be additive effects of several genes involved in regulating alcohol-related behaviors. Kinetic characteristics of aldehyde dehydrogenase and catalase in liver and brain of the C57BL/6J, DBA/2J, and BXD strains of mice were determined to test the hypothesis that the genetic regulation of the levels of alcohol-metabolizing enzymes mediate differences in VAC. Aldehyde dehydrogenase activity was determined spectrophotometrically by observing the change in absorption at 340 nm. Catalase activity was determined by measuring oxygen production with a Yellow Springs Biological Oxygen monitor and oxygen electrode. There was a strong negative relationship between VAC and brain catalase activity in the BXD RI and parental strains. These data suggest that RI strains are likely to be useful genetic models in the examination of quantitative trait loci controlling VAC and other responses to alcohol.	Gill K, Liu Y, Deitrich RA	Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism	Alcohol Clin Exp Res	20(1)	185-190	Feb	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8651451&dopt=Abstract	8651451		13	8 wks	56		MF	15-18	nMol NADH produced/minute/milligram of protein	1.89	0.14	2.02	0.14	0.57	0.05					1.47	0.19	0.59	0.11			0.95	0.15									1.43	0.16																			3.10	0.30							1.34	0.17																							7/11/2003	MK Sullivan	MK Sullivan										8651451.13
Proliferation of BrdU-labelled cells in subgranular zone, day 1 after last BrdU injection [number of cells]		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		02				MF	3-10	number of cells	5416	413.8	2014	377.3			2961	270.2			5389	521.6	7001	0.0															4047	243.9	2968	278.0											6131	1067.1			3515	227.5	2254	324.7	4227	1152.2																											6/14/2003		MK Sullivan										12153537.02
Survival of BrdU-labelled cells in subgranular zone, 4 weeks after last BrdU injection [number of cells]		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		03				MF	1-10	number of cells	2184	241.6	864	35.3			403	31.4	1157	213.4	2709	474.1	3745	391.4					1052	19.6									1085	15.7	1072	110.6											1283	156.1			1215	363.9	679	80.1	883	47.8																											6/14/2003		MK Sullivan										12153537.03
Number of neurons, 4 weeks after last BrdU injection [%] 		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		04				MF	1-10	%	78.3		51.8				27.9		63.7		67.6		78.6						44.4										57.7		68.7												79.2				68.8		50.5		56.9																												6/14/2003		MK Sullivan										12153537.04
Number of astrocytes, 4 weeks after last BrdU injection [%] 		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		05				MF	1-10	%	85.3		80.4				64.9		81.8		81.1		87.7						69.3										80.0		91.8												93.8				85.6		77.1		89.5																												6/14/2003		MK Sullivan										12153537.05
New neurons, 4 weeks after last BrdU, number of BrdU cells X ratio of NeuN / BrdU labelled cells		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		06				MF	1-10	number of BrdU cells X ratio of NeuN/BrdU labelled cells	1695	232.6	433	61.7			110	17.2	732	142.8	1816	393.3	2891	201.4					462	0.0									621	45.2	731	115.9											1007	153.8			872	355.6	365	81.4	493	27.2																											6/14/2003		MK Sullivan										12153537.06
Ethanol induced ataxia - initial sensitivity  Blood ethanol concentrations (BECo) at loss of balance on dowel test [mg %]		In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative sequencing analysis were used to compare cAMP response element binding protein (CREB) levels and protein-coding sequence, respectively. QTL analyses correlating strain means with allelic status at genetic markers identified several significant associations (p < 0.01). Analysis of variance revealed an effect of strain on behavioral and biochemical measures. There was a significant genetic correlation between initial sensitivity and basal cAMP accumulation in the cerebellum. We identified 6 provisional QTLs for initial sensitivity on four chromosomes, 6 provisional QTLs for AFT on four chromosomes, and 11 provisional QTLs for cAMP signaling on nine chromosomes. Two loci were found to overlap for measures of initial sensitivity and for cAMP signaling. Given the genetic correlation between initial sensitivity and basal cAMP accumulation, we investigated candidate genes in a QTL on chromosome 1. Comparative sequence analysis was performed, and protein levels were compared between C57 and DBA mice for Creb1. No significant differences were detected in coding sequence or protein levels for CREB. These results suggest that although ethanol sensitivity and cAMP signaling are determined by multiple genes, they may share certain genetic codetermination.	Kirstein SL, Davidson KL, Ehringer MA, Sikela JM, Erwin VG, Tabakoff B.	Quantitative trait loci affecting initial sensitivity and acute functional tolerance to ethanol-induced ataxia and brain cAMP signaling in BXD recombinant inbred mice	J Pharmacol Exp Ther	302(3)	1238-1245	Sep	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12183685&dopt=Abstract	12183685		09	55-80 days	55	80	Male	6-18	mg%	195.33	3.1	205.91	6.0	197.28	10.6	128.9	20.6	201.40	7.3	152.49	21.5	169.13	11.1	190.51	10.8	207.85	4.2	209.95	3.0	202.57	6.0	221.38	9.3	153.89	27.8	152.64	12.2	192.77	20.7	201.79	6.6	176.98	10.0	169.36	6.6	231.42	20.9			231.88	10.5	169.98	10.7			168.04	7.4	186.86	11.5	195.65	5.0	190.36	10.7	160.71	20.1	160.26	10.4			185.8	8.9					215.79	10.6	213.37	6.5	194.48	14.35			188.26	4.2			6/11/2003	MK Sullivan											12183685.09
New astrocytes, 4 weeks after last BrdU, number of BrdU cells X ratio of S100 beta / BrdU labelled cells		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		07				MF	1-101-10	number of BrdU cells X ratio of S100beta/BrdU labelled cells	136	32.2	245	30.9			142	15.9	243	168.1	404	170.2	326	177.2					255	0.0									235	48.1	245	26.2											179	52.1			165	50.3	183	22.6	290	60.3																											6/14/2003		MK Sullivan										12153537.07
Probe trial water maze time spent in target quadrant, day 5, %		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		08				MF	1-10	%	31.7	4.58	23.1	1.69			34.2	 2.76			37.7	8.25	28.6	6.85					34.4	0.00									28.1	8.79	31.4	3.71											35.1	5.30			30.5	4.20	24.9	4.30	32.2	6.35																											6/14/2003		MK Sullivan										12153537.08
Probe trial water maze time spent in swim path, day 5, %		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		09				MF	1-10	%	33.6	5.87	20.7	1.37			33.9	28.6			38.5	7.56	30.6	31.9					35.7	0.00									28.4	4.21	37.9	11.32											33.6	5.63			28.0	3.38	24.8	4.58	31.7	7.52																											6/14/2003		MK Sullivan										12153537.09
Latency water maze, day 6, seconds		A number of reports have indicated that adult neurogenesis might be involved in hippocampal function. While increases in adult neurogenesis are paralleled by improvements on learning tasks and learning itself can promote the survival of newly generated neurons in the hippocampus, a causal link between learning processes and adult hippocampal neurogenesis is difficult to prove. Here, we addressed the related question of whether the baseline level of adult neurogenesis is predictive of performance on the water maze task as a test of hippocampal function. We used ten strains of recombinant inbred mice, based on C57BL/6, which are good learners and show high baseline levels of neurogenesis, and DBA/2, which are known to be poor learners and which exhibit low levels of adult neurogenesis. Two of these strains, BXD-2 and BXD-8, showed a 26-fold difference in the number of newly generated neurons per hippocampus. Over all strains, including the parental strains, there was a significant correlation between the number of new neurons generated in the dentate gyrus and parameters describing the acquisition of the water maze task (slope of the learning curves). Similar results were seen when the parental strains were not included in the analysis. There was no correlation between adult hippocampal neurogenesis and probe trial performance, performance on the rotarod, overall locomotor activity, and baseline serum corticosterone levels. This result supports the hypothesis that adult neurogenesis is involved in specific aspects of hippocampal function, particularly the acquisition of new information.	Kempermann G, Gage FH	Genetic determinants of adult hippocampal neurogenesis correlate with acquisition, but not probe trial performance, in the water maze task.	Eur J Neurosci	16(1)	129-136	Jul	2002		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12153537&dopt=Abstract	12153537		10				MF	1-10	seconds	3.29	0.554	6.98	1.407			2.52	0.164			5.85	0.818	2.55	0.593					6.70	1.573									7.50	1.375	6.04	0.807											1.87	0.277			3.87	0.927	14.50	2.073	6.19	1.495																											6/14/2003		MK Sullivan										12153537.1
Mean raffinose undecaacetate (RUA) (0.4mM) consumed [%]	 	Thirty strains of mice were tested for their ability to taste a 0.4 mM solution of raffinose undecaacetate (RUA). There were large strain differences. Some strains showed little or no ability to taste the RUA. Two strains, SWR and Schneider, could taste RUA because they posses the Soaa allele which enables them to taste a variety of aceylated monosaccharides. Three other strains, BALB/c, DBA/2 and C3H, could taste RUA because they posses the RUAa allele which enables them to taste some larger structure which is a feature of the molecule as a whole. The gene Rua is tightly linked to the gene for quinine tasting. Qui, but the distribution of their alleles among the strains shows that they are different genes. It is suggested that there is in the mouse a cluster of tightly-linked genes, each one determining a taste receptor for a different bitter substance or chemical group. The relevance of these findings to the physiology of tasting is discussed.	Lush IE	The genetics of tasting in mice. IV. The acetates of raffinose, galactose, and beta-lactose	Genet Res	47(2)	117-123	Apr 	1986		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3754827&dopt=Abstract	3754827		01				MF	2-48	%							42	4.5			40	4.2			7	2.2			44	11.4							43	3.8	43	2.0	5	0.3					49	3.8							48	2.6	49	2.9	16	6.3	44	5.5	37	2.9	6	0.7																							7/14/2003		MK Sullivan										3754827.01
Mean beta-lactose acetate (0.3 mM) consumed [%]		Thirty strains of mice were tested for their ability to taste a 0.4 mm solution of raffinose undecaacetate (RUA). There were large strain differences. Some strains showed little or no ability to taste the RUA. Two strains, SWR and Schneider, could taste RUA because they posses the Soaa allele which enables them to taste a variety of aceylated monosaccharides. Three other strains, BALB/c, DBA/2 and C3H, could taste RUA because they posses the RUAa allele which enables them to taste some larger structure which is a feature of the molecule as a whole. The gene Rua is tightly linked to the gene for quinine tasting. Qui, but the distribution of their alleles among the strains shows that they are different genes. It is suggested that there is in the mouse a cluster of tightly-linked genes, each one determining a taste receptor for a different bitter substance or chemical group. The relevance of these findings to the physiology of tasting is discussed.	Lush IE	The genetics of tasting in mice. IV. The acetates of raffinose, galactose, and beta-lactose	Genet Res	47(2)	117-123	Apr 	1986		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3754827&dopt=Abstract	3754827		02				MF	1-14	%							6	2.4			18	8.5			30	6.4			7	1.6							11	5.5	3	0.8	34	10.2					16	8.2							19	5.1	17	4.7	36	4.3	6	1.0	15	4.0	34	4.6																							7/14/2003		MK Sullivan										3754827.02
Mean saccharin (3.2 mM) consumed [%]		Twenty-six strains of mice were tested for their reaction to four different sweet substances; saccharin, acesulfame, dulcin and sucrose. There was considerable strain variation in the degree to which they found the sweet substances preferable to water. The variation in preference for any one sweet substance is very highly correlated with the variation in preference for the other sweet substances. This is interpreted to mean that there is only one sweetness receptor, although an alternative explanation in terms of variation in psychological motivation is not discounted. The difference between C57BL/6Ty and DBA/2Ty is largely due to a single gene, Sac.	Lush IE	The genetics of tasting in mice. VI. Saccharin, acesulfame, dulcin and sucrose	Genet Res	53(2)	95-99	Apr	1989		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2744455&dopt=Abstract	2744455		01				MF		%					62	3.4	66	8.1	95	2.2	88	1.5	57	2.0			92	1.1	65	2.6					80	4.3	68	2.2	64	3.5	86	4.0					64	3.0			84	6.1	81	5.6	62	4.6	55	4.9	93	1.5	55		84	2.3	55	2.3																							7/14/2003		MK Sullivan										2744455.01
Mean acesulfame (3.2 mM) consumed [%]		Twenty-six strains of mice were tested for their reaction to four different sweet substances; saccharin, acesulfame, dulcin and sucrose. There was considerable strain variation in the degree to which they found the sweet substances preferable to water. The variation in preference for any one sweet substance is very highly correlated with the variation in preference for the other sweet substances. This is interpreted to mean that there is only one sweetness receptor, although an alternative explanation in terms of variation in psychological motivation is not discounted. The difference between C57BL/6Ty and DBA/2Ty is largely due to a single gene, Sac.	Lush IE	The genetics of tasting in mice. VI. Saccharin, acesulfame, dulcin and sucrose	Genet Res	53(2)	95-99	Apr	1989		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2744455&dopt=Abstract	2744455		02				MF		%					53	1.7	57	4.1	93	2.7	82	2.2	58	2.0			89	3.8	57	4.9					81	2.6	57	1.7	60	1.3	77	2.8					56	2.6			79	1.0	77	2.7	54	3.8	51	3.2	85	1.9	53		88	2.0	52	2.6																							7/14/2003		MK Sullivan										2744455.02
Mean glycine (10 mM) consumed [%]		Glycine tastes both bitter and sweet to mice but there are differences between strains in their ability to detect each taste. With respect to the bitter taste, fifteen strains were classified as tasters and twelve strains as non-tasters. The difference is due to a single gene, Glb (glycine bitterness). Cyclohexamide tastes bitter to all mice at a concentration of 8 µM, but strain differences in sensitivity to the taste of cycloheximide can be detected at lower concentrations. The BXD RI strains can be classified into two groups with respect to sensitivity to cycloheximide. This is probably due to the segregation of two alleles of a single gene, Cyx. A comparison of the distribution in RI strins of alleles of four bitterness-tasting genes shows that the loci are all closely linked and are probably in the order Cyx-Qui-Rua-Glb.    	Lush IE, Holland G	The genetics of tasting in mice. V. Glycine and cycloheximide	Genet Res	52(3)	207-212	Dec	1988		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3243425&dopt=Abstract	3243425		01				MF	3-28	%					6	0.7	32	6.0	8	4.4	34	5.0	13	2.1			7	2.3	31	3.0					4	1.4	33	4.0	45	5.6	7	2.1					42	2.4			4	1.6	9	3.0	35	7.4	36	2.6	4	0.3	35	5.6	39	5.8	6	2.2																							7/14/2003		MK Sullivan										3243425.01
B-mannosidase activity in kidney of Female [mg p-nitrophenl liberated/g tissue wet weight/hr at 37 degrees C]		A gene (Bmn) with a major effect on beta-mannosidase activity in kidney and liver of the house mouse was revealed by assay with the synthetic substrate p-nitrophenyl-beta-D-mannoside. Activity is low in DBA/2J and CSB mice and high in C57BL/6J mice. By the use of the BXD series of recombinant inbred strains and by crosses between C57BL and CSB, it was possible to map the gene to the distal part of chromosome 3 by demonstration of linkage to a gene for cadmium resistance, cdm, as well as to the Adh-3 locus.	Lundin LG	A gene (Bmn) controlling B-mannosidase activity in the mouse is located in the distal part of chromosome 3	Biochem Genet 	25(7-8)	603-610 	Aug	1987 		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3447593&dopt=Abstract	3447593		02				Female		mg p-nitrophenl liberated/g tissue wet weight/hr at 37 degrees C	2.710		1.505		3.341		2.011		3.473		3.290		0.030		3.558		1.680		2.027				2.643		3.093		1.420		2.097		0.299				2.062		3.789				2.808		1.679		4.234		2.001		3.614				3.252		1.479																								7/14/2003	MK Sullivan	MK Sullivan										3447593.02
Growth of Salmonella typhimurium bacteria strain LT2-Z from livers and spleens 6 days post inoculation with 102 CFU [log10 number of CFU] 		The studies described in this paper provide evidence that the pathogenesis of Salmonella typhimurium in mice is dependent on interactions between particular genotypes of the infected mice and the infecting Salmonella strain. This conclusion was based on data obtained by infecting a panel of BXD recombinant inbred mice with each of three S. typhimurium strains. One of the S. typhimurium strains was a transconjugant (WB500) produced in an interrupted mating between the two other strains, one (SR-11) of high and the other (LT2-Z) of low virulence for BALB/c mice. We found that strain WB500 appeared to have inherited from SR-11 a gene (or genes) which was required to exploit the Itys/s genotype in mice. However, WB500 apparently lacked other SR-11 virulence gene(s), whose effect on the in vivo growth of SR-11 was independent of the Ity genotype of the mouse.	Benjamin WH Jr, Turnbough CL Jr, Posey BS, Briles DE	Salmonella typhmurium virulence genes necessary to exploit the Itys/s genotype of the mouse	Infect Immun	51(3)	872-878	Mar	1986		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3512437&dopt=Abstract	3512437 		01	8-12 wks	56	84	MF	4 or more	log10 number of CFU	4.92	0.218	5.55	0.235	4.14	0.166	5.29	0.274	6.79	0.560	4.12	0.071	4.69	0.154	4.95	0.149	4.89	0.174	4.57	0.174	5.42	0.262	5.17	0.287			3.04	0.154	5.61	0.118									3.78	0.215	5.52	0.332					4.82	0.104	3.06	0.235	4.69	0.107			3.78	0.283																							7/15/2003	MK Sullivan	MK Sullivan										3512437.01
Growth of Salmonella typhimurium bacteria strain WB500 from livers and spleens 6 days post inoculation with 102 CFU [log10 number of CFU] 		The studies described in this paper provide evidence that the pathogenesis of Salmonella typhimurium in mice is dependent on interactions between particular genotypes of the infected mice and the infecting Salmonella strain. This conclusion was based on data obtained by infecting a panel of BXD recombinant inbred mice with each of three S. typhimurium strains. One of the S. typhimurium strains was a transconjugant (WB500) produced in an interrupted mating between the two other strains, one (SR-11) of high and the other (LT2-Z) of low virulence for BALB/c mice. We found that strain WB500 appeared to have inherited from SR-11 a gene (or genes) which was required to exploit the Itys/s genotype in mice. However, WB500 apparently lacked other SR-11 virulence gene(s), whose effect on the in vivo growth of SR-11 was independent of the Ity genotype of the mouse.	Benjamin WH Jr, Turnbough CL Jr, Posey BS, Briles DE	Salmonella typhmurium virulence genes necessary to exploit the Itys/s genotype of the mouse	Infect Immun	51(3)	872-878	Mar	1986		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3512437&dopt=Abstract	3512437 		02	8-12 wks	56	84	MF	4 or more	log10 number of CFU	6.67	0.230	5.04	0.305	4.29	0.559	7.74	0.222	7.64	0.305	3.96	0.182	4.69	0.096	6.75	0.363	7.84	0.164	6.61	0.433	5.27	0.181	8.16	0.000			3.69	0.000	7.78	0.198									4.08	0.205	6.46	0.778					4.86	0.083	3.86	0.098	5.16	0.076			3.91	0.069																							7/15/2003	MK Sullivan	MK Sullivan										3512437.02
Growth of Salmonella typhimurium bacteria strain SR-11 from livers and spleens 6 days post inoculation with 102 CFU [log10 number of CFU] 		The studies described in this paper provide evidence that the pathogenesis of Salmonella typhimurium in mice is dependent on interactions between particular genotypes of the infected mice and the infecting Salmonella strain. This conclusion was based on data obtained by infecting a panel of BXD recombinant inbred mice with each of three S. typhimurium strains. One of the S. typhimurium strains was a transconjugant (WB500) produced in an interrupted mating between the two other strains, one (SR-11) of high and the other (LT2-Z) of low virulence for BALB/c mice. We found that strain WB500 appeared to have inherited from SR-11 a gene (or genes) which was required to exploit the Itys/s genotype in mice. However, WB500 apparently lacked other SR-11 virulence gene(s), whose effect on the in vivo growth of SR-11 was independent of the Ity genotype of the mouse.	Benjamin WH Jr, Turnbough CL Jr, Posey BS, Briles DE	Salmonella typhmurium virulence genes necessary to exploit the Itys/s genotype of the mouse	Infect Immun	51(3)	872-878	Mar	1986		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3512437&dopt=Abstract	3512437 		03	8-12 wks	56	84	MF	5 or more	log10 number of CFU	8.01	0.091	6.23	0.104	5.28	0.062	7.35	0.077	7.81	0.115	5.58	0.068	4.86	0.196	7.92	0.184	7.46	0.083	7.54	0.215	5.38	0.084					7.27	0.277	8.04										5.27	0.073	8.05	0.071					6.31	0.083	5.62	0.195	5.57	0.082			5.42	0.099																							7/15/2003	MK Sullivan	MK Sullivan										3512437.03
Virus titer in spleen 4 days after infection with 5X104 PFU of MCMV [log10 mean titer]		The resistance of mice to lethal infection by murine CMV (MCMV) is under complex host genetic control with contributions from both H-2 and non-H-2 genes. We have previously shown that an autosomal, non-MHC encoded gene, Cmv-1, controls MCMV replication in the spleen. We have investigated the mechanism by which the Cmv-1 resistance gene confers protection against MCMV infection. Using H-2 compatible irradiation bone marrow chimeras, the enhanced resistance to MCMV infection that is associated with the Cmv-1l allele in the C57BL background was shown to be mediated by an irradiation-sensitive bone marrow-derived cell population, or a factor produced by these cells. The lack of correlation between serum IFN titers and the strain distribution pattern of Cmv-1 in CXB recombinant inbred mouse strains suggests that IFN does not mediate resistance conferred by this gene. Similarly, the lack of effect of in vivo depletion of mature CD4+ and CD8+ T cells on virus replication in C57BL/6J mice indicates that T cells are unlikely to be involved. In contrast, in vivo depletion of NK cells by injection of the anti-NK1.1 mAb PK136 abrogated restricted splenic virus replication in C57BL/6J----BALB.B chimeric mice and in the Cmv-1l CXB strains. These data indicate that the effect of the Cmv-1 gene is mediated by NK cells. The significant augmentation in NK cell activity after MCMV infection of the susceptible Cmv-1h strains (BALB/cBy), CXBG/By, CXBH/By, CXBI/By, and CXBK/By) indicates the existence in these mice of NK cells that are functionally and phenotypically distinct from those in Cmv-1l strains. NK cells present in the Cmv-1h strains are unable to restrict efficiently splenic MCMV replication in vivo, possibly due to a lack of specificity for virus-infected target cells. Finally, flow cytometric analysis of NK1-1 expression in CXB and BXD RI mice together with MCMV replication studies in the BXD RI strains indicate that Cmv-1 is closely linked to NK1.1 and other loci that reside on a distal segment of murine chromosome 6 in a region that has recently been defined as the natural killer complex.	Scalzo AA, Fitzgerald NA, Wallace CR, Gibbons AE, Smart YC, Burton RC, Shellam GR 	The effect of the Cmv-1 resistance gene, which is linked to the natural killer cell gene complex, is mediated by natural killer cells.	J Immunol	149(2)	581-589	July 	1992		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1378069&dopt=Abstract	1378069 		01	8-12 wks	56	84	Females	4	Log10 mean titer	2.10	0.081	4.60	0.071	4.25	0.034			4.64	0.040	1.30	0.040	5.20	0.050	4.72	0.083	4.91	0.057	1.66	0.122	5.42	0.110			5.20	0.086	1.30	0.042	1.31	0.047	5.48	0.052	1.31	0.040	1.66	0.149	1.30	0.043	1.29	0.035	4.65	0.043			2.23	0.154	1.30	0.044	5.26	0.073	1.49	0.066	1.74	0.127	4.62	0.149																		                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             					7/15/2003	Mk Sullivan	MK Sullivan										1378069.01
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone (11.1B/c) [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		01				MF		cpm					412						17161		795		38026				281				337						292								765						22049		29821		29808				15452																																								1697877.01
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone D9 [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		02				MF		cpm					260						11245		205		4758				194				220						156								432						11748		4883		15283				8478																																								1697877.02
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone E4.3 [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		03				MF		cpm					318						7345		336		12950				328				251						139								299						6293		4343		4662				5170																																								1697877.03
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone 11.4 B/c [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		04				MF		cpm					221						145		161		173				25194										17405								457						304		6760		8570				8299																																								1697877.04
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone TGVH 9 [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		05				MF		cpm					13801						463		235		407				387				359						424								38485						12698		134		158				47300																																								1697877.05
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- T-cell clone TGVH32 [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		06				MF		cpm					21536						656		575		201				249				335						465								32232						20878		425		169				18342																																								1697877.06
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4-CD8+ H-2(d) specific T-cell clone F10 ECK [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		07				MF		cpm					5234						3138		340		3766				5407				289						2580								5023						4804		2413		2244				4130																																								1697877.07
Antigenic activity of irradiated BXD spleen cells for Thy-1+CD3+CD4+CD8- Mls(a) specific T-cell clone F5J10  [Thymidine uptake cpm]		The relative contribution of individual non-H-2 Ag and of T cell subsets that initiate graft-vs-host reaction (GVHR) as well as the mechanism responsible for histopathologic lesions are still a matter of debate. To address these questions and to favor the selection of T cells primed in vivo against non-H-2 Ag important in GVHR we derived T cell clones from spleens of (DBA/2 x B10.D2)F1 (H-2d) mice developing this reaction after the graft of B10.D2 (H-2d) cells incompatible for numerous non-H-2 Ag plus Mlsa. The pattern of reactivity of eight selected clones against cells from different strains of mice including (BXD)RI strains indicated that one CD4+ clone is specific for Mlsa and seven additional clones (six CD4+ and one CD8+) are specific for four different non-H-2 Ag (Ag.I-IV) and proliferate in an H-2-restricted manner. The same series of experiments suggested that Ag.I and II are poorly polymorphic and allowed to propose the localisation of the genes controlling Ag.I (chromosome 1) and Ag.III (chromosome 4). All the clones show a triple (alpha, beta, gamma) mRNA transcript for TCR but at their surface they express the alpha/beta-heterodimer. The clone specific for Mlsa expresses V beta 6 and that specific for Ag.IV expresses V beta 8.1. Rapid mortality accompanied by clinical and histologic signs of severe GVHR was observed after administration of CD4+ clones (together with host-syngeneic bone marrow) derived early after grafting and specific for Ag.I and II but not after administration of: 1) CD8+ cytolytic clone derived early after grafting and specific for Ag.IV; 2) CD4+ clones derived late after grafting and specific for Ag.III; and 3) CD4+ clone specific for Mlsa. A clear correlation was established between the capacity of CD4+ clones to induce GVHR mortality, to mediate host-specific DTH and to release a high level of TNF. In conclusion: 1) the reaction against a single non-H-2 Ag is sufficient to provoke lethal GVHR; 2) the capacity to provoke GVHR mortality depends on antigenic specificity and functional properties of the responding clones; 3) the inflammatory process mediated by CD4+ clones may play a major role whereas the specific CD8+ T cell-mediated cytolytic activity is not necessarily lethal.	Miconnet I, Huchet R, Bonardelle D, Motta R, Canon C, Garay-Rojas E, Kress M, Reynes M, Halle-Pannenko O, Bruley-Rosset M.	Graft-versus-host mortality induced by noncytolytic CD4+ T cell clones specific for non-H-2 antigens	J Immunol	145(7)	2123-2131	Oct	1990		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1697877&dopt=Abstract	1697877		08				MF		cpm					266						259		12535		7934				109										261								6819						14339		9057		18358				18635																																								1697877.08
Blood glucose levels preinjection with 4g/kg of ethanol in females [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		02				Female	0-14	mg/dl	103.8	6.0	88.3	3.1			88.0	6.4			99.0	4.6	100.3	6.0			102.0	6.1	80.0	3.1	100.0	7.5	95.3	1.7	85.8	8.4	77.9	2.6	86.1	2.7	85.3	3.2			104.2	4.9									100.6	2.3			100.1	2.1	87.2	3.5			89.4	3.4																							7/23/2003		MK Sullivan										12766619.02
Blood glucose levels preinjection with 4g/kg of ethanol in males [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		03				Male	0-10	mg/dl	122.7	6.7	98.3	4.7			87.8	1.9			112.1	3.5	108.5	7.4	113.2	3.7	109.5	3.2	86.0	3.8	106.2	4.0	111.6	5.4	81.3	6.3	89.7	2.7	84.3	4.1	89.6	3.4			121.5	3.3			95.0	8.5									105.2	4.6			112.7	10.1	87.8	4.4																							7/23/2003		MK Sullivan										12766619.03
Blood glucose levels postinjection (120 min) with 4g/kg  of ethanol in females [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		04				Female	0-14	mg/dl	163.0	28.9	117.8	3.0			127.7	6.1			137.0	14.1	138.6	9.9			105.2	7.8	125.9	5.6	113.0	16.1	120.3	4.7	76.2	5.6	109.3	6.0	106.7	3.2	111.3	10.7			127.7	6.2									113.0	3.2			132.0	9.8	95.2	8.4			110.1	5.9																							7/23/2003		MK Sullivan										12766619.04
Blood glucose levels postinjection (120 min) with 4g/kg  of ethanol in males [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		05				Male	0-10	mg/dl	234.2	23.9	152.5	7.5			166.6	22.8			155.0	8.0	187.0	7.7	184.7	3.1	138.2	9.9	118.4	7.3	130.2	17.5	138.3	6.9	119.0	20.1	137.0	6.6	111.1	8.7	151.4	9.8			231.9	12.3			149.0	15.0									188.6	13.9			182.2	6.3	140.0	8.4																							7/23/2003		MK Sullivan										12766619.05
Blood glucose levels preinjection with saline in females [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		06				Female	0-14	mg/dl	105.4	6.5	90.0	3.5			93.4	3.7			94.2	4.8	102.7	3.4			100.0	0.0	87.1	2.7	87.7	7.8	70.3	10.7	81.6	10.3	77.8	3.5	83.5	2.4	82.2	4.0			98.4	2.9									95.8	4.3			102.1	5.5					86.5	3.7																							7/23/2003		MK Sullivan										12766619.06
Blood glucose levels preinjection with saline in males [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		07				Male	0-10	mg/dl	117.8	3.8	104.0	4.6			95.6	4.5			113.2	4.3	120.0	24.0	107.5	1.4	102.2	4.3	87.5	5.2	114.0	3.3	109.6	6.9	77.7	4.5	92.6	3.5	86.0	4.6	90.2	5.1			125.6	9.1			101.7	6.9									105.5	4.2					86.1	6.0																							7/23/2003		MK Sullivan										12766619.07
Blood glucose levels postinjection (120 min) with saline in females [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		08				Female	0-14	mg/dl	119.6	7.9	99.3	5.9			102.4	5.1			103.9	6.5	114.7	4.1			109.3	4.7	101.8	4.6	109.3	5.9	106.3	14.7	71.6	4.3	82.1	5.6	92.6	3.5	99.2	7.3			112.6	10.2									114.6	3.5			104.0	4.4					93.9	4.4																							7/23/2003		MK Sullivan										12766619.08
Blood glucose levels postinjection (120 min) with saline in males [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		09				Male	0-10	mg/dl	140.8	11.0	117.2	3.1			121.6	4.9			130.4	3.7	145.0	10.0	120.7	4.0	130.0	10.4	103.4	7.2	118.0	5.1	104.3	1.4	86.1	8.3	90.3	5.2	90.0	5.7	108.5	6.2			154.0	8.6			143.0	15.1									111.2	4.0					101.6	10.2																							7/23/2003		MK Sullivan										12766619.09
Body temperature preinjection with 4 g/kg of ethanol in females [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		10				Female	0-15	degrees C	37.4	0.3	37.7	0.3			37.7	0.3			37.4	0.3	37.4	0.3			37.5	0.7	37.8	0.2	37.4	0.1	37.4	0.6	37.1	0.4	36.9	0.3	37.3	0.2	37.2	0.4			37.8	0.3									37.9	0.2			37.7	0.3	37.2	0.4	37.3	0.3	37.1	0.3																							7/23/2003		MK Sullivan										12766619.1
Body temperature preinjection with 4 g/kg of ethanol in males [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		11				Male	0-10	degrees C	37.3	0.5	37.4	0.3			37.4	0.4			36.9	0.3	36.9	0.5	37.6	0.5	37.7	0.4	37.1	0.5	37.0	0.4	37.0	0.4	36.0	0.7	36.9	0.3	36.7	0.3	37.0	0.5			37.5	0.3			36.9	0.7									37.8	0.5			37.5	0.5	37.0	0.5																							7/23/2003		MK Sullivan										12766619.11
Body temperature postinjection (120 min) with 4 g/kg of ethanol in females [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		12				Female	0-15	degrees C	34.4	0.3	33.8	0.3			34.1	0.3			34.1	0.4	35.1	0.3			36.1	0.4	33.1	0.2	35.4	0.5	34.1	0.5	34.1	0.4	35.2	0.3	34.7	0.1	34.2	0.3			34.9	0.2									35.6	0.3			34.9	0.1	35.4	0.3	34.9	0.4	33.0	0.5																							7/23/2003		MK Sullivan										12766619.12
Body temperature postinjection (120 min) with 4 g/kg of ethanol in males [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		01				Male	0-10	degrees C	34.7	0.2	33.5	0.3			33.8	0.3			33.9	0.3	34.8	0.5	34.8	0.2	35.4	0.2	33.6	0.5	34.2	0.4	33.2	0.7	34.2	0.4	34.8	0.3	34.4	0.2	34.1	0.5			34.4	0.2			34.0	0.4									35.1	0.1			34.5	0.5	34.0	0.4																							7/23/2003		MK Sullivan										12766619.01
Body temperature preinjection with saline in females [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		13				Female	0-15	degrees C	37.4	0.5	37.7	0.1			37.7	0.4			37.1	0.4	37.3	0.3			37.9	0.4	37.9	0.2	37.5	0.5	37.4	0.9	37.0	0.3	36.9	0.3	37.3	0.2	37.1	0.5			37.4	0.3									37.8	0.2			37.5	0.4	37.0	0.4	37.5	0.3	37.5	0.3																							7/23/2003		MK Sullivan										12766619.13
Body temperature preinjection with saline in males [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		14				Male	0-10	degrees C	37.1	0.6	37.0	0.5			37.7	0.4			37.0	0.3	37.2	0.4	37.3	0.7	37.6	1.0	37.1	0.4	37.7	0.3	37.3	0.6	36.5	0.4	37.0	0.3	36.6	0.3	36.9	0.5			37.6	0.4			36.8	0.6									37.8	0.4			37.7	0.7	37.1	0.5																							7/23/2003		MK Sullivan										12766619.14
Body temperature postinjection (120 min) with saline in females [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		15				Female	0-15	degrees C	37.2	0.4	37.6	0.1			37.5	0.3			36.9	0.3	37.3	0.2			38.5	0.2	37.8	0.2	37.8	0.1	37.8	0.3	37.5	0.2	37.0	0.2	37.4	0.1	37.0	0.2			37.9	0.1									37.8	0.2			37.4	0.2	36.4	0.5	37.4	0.2	37.6	0.2																							7/23/2003		MK Sullivan										12766619.15
Body temperature postinjection (120 min) with saline in males [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		16				Male	0-10	degrees C	37.4	0.3	37.5	0.2			37.2	0.4			37.2	0.1	37.2	0.4	36.5	0.8	37.6	0.6	37.6	0.3	37.7	0.1	37.6	0.7	37.1	0.4	37.2	0.1	37.3	0.3	37.2	0.2			37.3	0.2			37.4	0.4									37.2	0.3			38.1	0.4	37.5	0.3																							7/23/2003		MK Sullivan										12766619.16
Blood glucose difference [postinjection minus preinjection (4g/kg ethanol test)] female [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		17				Female	0-14	mg/dl	60.3	24.2	30.0	1.3			40.4	6.3			38.6	10.8	40.0	7.4			4.1	9.0	47.0	5.1	13.2	8.3	25.7	5.8	-10.3	11.4	32.0	6.4	21.1	8.8	26.3	9.8			24.1	4.5									12.3	4.2			32.2	10.0	8.2	5.9			20.9	4.29																							7/23/2003		MK Sullivan										12766619.17
Blood glucose difference [postinjection minus preinjection (4g/kg ethanol test)] male [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		18				Male	0-10	mg/dl	112.8	22.9	54.8	6.1			79.1	21.9			43.6	7.6	79.5	7.6	72.3	4.6	29.2	10.2	33.3	8.1	24.2	14.6	27.1	10.1	36.4	14.7	50.2	5.2	27.1	8.5	62.8	10.8			111.7	10.3			5.5	13.7									84.3	11.6			70.0	13.0	52.7	6.9																							7/23/2003		MK Sullivan										12766619.18
Blood glucose difference [postinjection minus preinjection (saline test)] female [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		19				Female	0-14	mg/dl	14.7	7.1	10.2	7.1			9.0	5.4			10.2	7.9	12.1	5.5			9.6	4.4	15.2	5.1	22.2	13.0	36.8	7.3	-10.6	9.4	4.76	6.6	9.2	3.9	17.5	10.0			14.6	8.0									18.9	5.9			2.2	5.6					7.4	6.2																							7/23/2003		MK Sullivan										12766619.19
Blood glucose difference [postinjection minus preinjection (saline test)] male [mg/dl]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		20				Male	0-10	mg/dl	23.0	11.6	13.1	4.5			26.2	7.2			17.9	3.7	25.2	13.8	13.4	4.3	28.6	9.5	16.1	9.7	4.1	2.5	-5.4	5.9	8.7	5.8	-2.4	4.9	3.4	6.0	18.2	2.6			28.7	7.2			41.6	7.9									5.6	4.1					15.5	7.5																							7/23/2003		MK Sullivan										12766619.2
Body temperature difference [postinjection minus preinjection (4 g/kg ethanol test)] female [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		21				Female	0-15	degrees C 	-2.9	0.5	-3.8	0.4			-3.6	0.5			-3.2	0.5	-2.3	0.4			-1.4	0.6	-4.6	0.3	-2.0	0.5	-3.3	0.7	-2.9	0.4	-1.7	0.3	-2.6	0.2	-3.0	0.4			-2.9	0.3									-2.4	0.3			-2.8	0.4	-1.8	0.5	-2.3	0.5	-4.1	0.8																							7/23/2003		MK Sullivan										12766619.21
Body temperature difference [postinjection minus preinjection (4 g/kg ethanol test)] male [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		22				Male	0-10	degrees C 	-2.3	0.6	-3.9	0.5			-3.6	0.6			-3.0	0.6	-2.0	0.8	-2.8	0.7	-2.2	0.6	-3.5	0.4	-2.8	0.7	-3.9	0.6	-1.9	1.0	-2.1	0.5	-2.3	0.3	-2.9	0.8			-3.1	0.3			-2.9	0.6									-2.7	0.5			-3.0	0.9	-3.0	0.7																							7/23/2003		MK Sullivan										12766619.22
Body temperature difference [postinjection minus preinjection (saline test)] female [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		23				Female	0-15	degrees C 	-0.2	0.4	-0.1	0.1			-0.1	0.3			-0.2	0.4	-0.1	0.1			0.6	0.2	-0.1	0.1	0.4	0.5	0.4	0.6	0.5	0.2	0.1	0.2	0.0	0.2	0.1	0.4			0.5	0.2									0.1	0.1			0.1	0.3	-0.6	0.6	-0.1	0.2	0.1	0.2																							7/23/2003		MK Sullivan										12766619.23
Body temperature difference [postinjection minus preinjection (saline test)] male [degrees C]		BACKGROUND:Genetic sensitivity to ethanol-induced hyperglycemia was hypothesized to be related to sensitivity to ethanol-induced hypothermia and conditioned taste aversion. These hypotheses were explored by characterizing blood glucose changes after ethanol exposure in BXD recombinant inbred mice.METHODS:Adult male and female BXD recombinant inbred mice were acutely exposed to 4 g/kg of ethanol or saline with the order of exposure counterbalanced, and separated by a 1-week interval. Tail blood samples and rectal temperatures were determined immediately before ethanol/saline exposure and 2 hr after exposure.RESULTS:Substantial strain differences in ethanol-induced hyperglycemia and hypothermia were noted. In addition, sex also determined sensitivity to ethanol-induced hyperglycemia and interacted with strain. Correlational analyses using strain means indicated that ethanol-induced hyperglycemia was genetically independent from ethanol-induced hypothermia or conditioned taste aversion. Quantitative trait locus (QTL) analyses indicated provisional QTL for ethanol-induced hyperglycemia on chromosomes 1, 3, 4, 6, 7, 9, 12, 14, and 18, which, in part, were sex specific.CONCLUSIONS:These findings indicate important sex differences in the glycemic response to ethanol. In addition, multiple genes likely control this response, independent from genes that are important for the thermic or aversive effects of ethanol.	Risinger FO	Genetic analyses of ethanol-induced hyperglycemia	Alcohol Clin Exp Res	27(5)	756-764	May	2003		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12766619&dopt=Abstract	12766619		24				Male	0-10	degrees C 	0.3	0.4	0.5	0.3			-0.5	0.4			0.3	0.2	-0.1	0.2	-0.7	1.0	0.1	1.1	0.5	0.2	0.1	0.2	0.2	0.4	0.6	0.2	0.2	0.2	0.6	0.4	0.3	0.3			-0.3	0.2			0.7	0.4									-0.6	0.3			0.4	0.3	0.4	0.6																							7/23/2003		MK Sullivan										12766619.24
Thymic T-cell response to anti-CD3-induced proliferation		Thymic and peripheral T-cells from NOD mice display a proliferative unresponsiveness on stimulation through the T-cell receptor/CD3 complex. Interleukin 4 reverses NOD T-cell unresponsiveness in vitro and prevents the onset of diabetes in vivo, suggesting a causal relationship between the T-cell unresponsiveness and diabetes susceptibility in NOD mice. Both quantitative trait loci analysis of BXD recombinant inbred mice and linkage analysis of NOD outcross populations reveal that the control of NOD thymic T-cell proliferative unresponsiveness genetically maps to a central region on mouse chromosome 11, which includes the beta-chemokine gene family. This finding raises the possibility that a beta-chemokine(s) may regulate T-cell unresponsiveness as well as diabetes susceptibility in NOD mice.	Gill BM, Jaramillo A, Ma L, Laupland KB, Delovitch TL	Genetic linkage of thymic T-cell proliferative unresponsiveness to mouse chromosome 11 in NOD mice: A possible role for chemokine genes	Diabetes	44(6)	614-619	Jun	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7789623&dopt=Abstract	7789623			8-12 wks	56	84	Female	3-10						17.99	2.841	29.53	3.707	2.84	0.000	34.51	6.017	43.11	10.593	4.20	1.222	27.22	6.541	2.66	0.000	33.20	6.967	7.65	1.441	2.37	0.000	4.86	0.000	17.19	5.185	3.07	0.000	1.83	0.000	3.29	0.000	5.07	1.037	40.15	8.259	22.96	7.859	17.36	1.852	27.61	7.076	5.54	3.712	5.04	1.356	31.48	6.991	47.96	9.041	8.45	1.833																							7/23/2003		MK Sullivan										7789623
Total distance traveled 1 hour after 7.5 mg/kg PCP injection minus total distance traveled in response to 0.9% saline injection 1 hour prior to 7.5 mg/kg PCP injection [cm] 		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		01	8-12 wks	56	84	Female	7-17	cm	5525	631.7	5062	1135.4	4897	1048.2	4616	1123.2	612	329.3	4695	675.6	982	767.1	441	395.7	10276	1773.2	10420	1487.8	8905	980.5	2267	884.1	2620	486.6	3237	687.8	2999	824.4	6160	1495.1	12184	2443.9	688	419.5	4218	761.0	8182	1141.5	1165	323.2	6391	1658.5	1159	458.5	245	98.8	2633	876.8	2805	761.0	5463	1791.5	3298	1423.8																							8/1/2003		MK Sullivan										8914121.01
Total distance traveled 1 hour after 7.5 mg/kg PCP injection [cm]		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		02	8-12 wks	56	84	Female	7-17	cm	6180		5274		6307		5459		1487		5691		3709		1499		10922		12818		2999		2743		3011		4322		3763		6456		11556		1873		4541		7795		1426		7287		2635		684		4337		3938		6035		4701																								8/1/2003		MK Sullivan										8914121.02
Distance traveled in response to 0.9% saline injection 1 hour prior to injection of 7.5 mg/kg PCP [cm]		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		03	8-12 wks	56	84	Female	7-17	cm	605		273		2029		957		361		1062		1980		1184		718		2416		245		560		532		1123		751		209		659		1294		609		1615		284		988		443		442		1847		1037		663		1598																								8/1/2003		MK Sullivan										8914121.03
Total distance traveled 1 hour after 5 mg/kg amphetamine injection minus total distance traveled in response to 0.9% saline injection 1 hour prior to 5 mg/kg amphetamine injection [cm]		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		04	8-12 wks	56	84	Female	7-17	cm	4844	1030.7	7801	1036.0	13196	1959.4	4389	631.4	6627	983.1	8699	1848.3	2973	911.1	8065	714.3	2881	766.3	2461	910.3	5670	1097.3	4267	1072.8	9238	2406.1	414	337.2	4438	1319.5	8887	2070.5	4821	780.1	9263	658.2	6573	749.4	5800	1051.3	10645	1578.5	8489	1993.1	15450	2591.6	4772	606.9	4507	1135.6	4413	744.8	5166	908.8	6022	1511.1																							8/1/2003		MK Sullivan										8914121.04
Total distance traveled 1 hour after 5 mg/kg amphetamine injection [cm]		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		05	8-12 wks	56	84	Female	7-17	cm	6251		7137		14117		4990		6820		10392		4061		9382		3238		3389		6222		5243		9746		1756		5539		9105		5021		10467		6910		6730		10844		10070		15944		5005		5479		5925		5533		6867																								8/1/2003		MK Sullivan										8914121.05
Distance traveled in response to 0.9% saline injection 1 hour prior to injection of 5 mg/kg amphetamine [cm]		Phencyclidine (PCP) and amphetamine (AMP) can induce psychotic syndromes in humans, whereas administration of these drugs to mice results in behavioral activation that is influenced by genetic factors. Quantitative trait loci (QTL) underlying genetic differences in response to PCP and AMP in mice were provisionally identified by correlating allelic variation at known marker loci in the BXD series of recombinant inbred (RI) mice and its progenitors (C57BL/6J and DBA/2J inbred strains) with the locomotor response of each strain to PCP and AMP. Total distance traveled for individual mice from each of the 26 BXD RI and two progenitor strains was measured after injections of normal saline and 7.5 mg/kg i.p. injection of PCP. This procedure was repeated after 1 week, using 5.0 mg/kg of AMP, instead of PCP. Markers significantly (p < .01) correlated with response to PCP map to murine chromosomes 1, 14, and 15. Response to amphetamine was correlated with markers mapping to chromosomes 4, 5, 6, 8, 14, and 18. Identification of the QTL underlying PCP-induced and AMP-induced behavior in mice may provide clues into the complicated genetics of psychosis in humans.	Alexander RC, Wright R, Freed W	Quantitative trait loci contributing to phencyclidine-induced and amphetamine-induced locomotor behavior in inbred mice.	Neuropsychopharmacology	15(5)	484-490	Nov	1996		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8914121&dopt=Abstract	8914121		06	8-12 wks	56	84	Female	7-17	cm	841		431		996		911		423		1795		798		1465		413		1090		582		592		645		1565		1195		201		314		1370		642		688		202		1789		586.2		277		1074		1143		460		1003																								8/1/2003		MK Sullivan										8914121.06
Mean tumor multiplicity in liver after infection with 0.01 ml/g body wt N,N-diethylnitrosamine [number of tumors]		Male DBA/2J mice are approximately 20-fold more susceptible than male C57BL/6J mice to hepatocarcinogenesis induced by perinatal treatment with N,N-diethylnitrosamine (DEN). In order to elucidate the genetic control of hepatocarcinogenesis in DBA/2J mice, male BXD recombinant inbred, D2B6F1 x B6 backcross, and D2B6F2 intercross mice were treated at 12 days of age with DEN and liver tumors were enumerated at 32 weeks. Interestingly, the distribution of mean tumor multiplicities among BXD recombinant inbred strains indicated that hepatocarcinogen-sensitive DBA/2 mice carry multiple genes with opposing effects on the susceptibility to liver tumor induction. By analyzing D2B6F1 x B6 backcross and D2B6F2 intercross mice for their liver tumor multiplicity phenotypes and for their genotypes at simple sequence repeat marker loci, we mapped two resistance genes carried by DBA/2J mice, designated Hcr1 and -2, to chromosomes 4 and 10, respectively. Hcr1 and Hcr2 resolved the genetic variance in the backcross population well, indicating that these resistance loci are the major determinants of the variance in the backcross population. Although our collection of 100 simple sequence repeat markers allowed linkage analysis for approximately 95% of the genome, we failed to map any sensitivity alleles for DBA/2J mice. Thus, it is likely that the susceptibility of DBA/2J mice is the consequence of the combined effects of multiple sensitivity loci.	Lee GH, Bennett LM, Carabeo RA, Drinkwater NR	Identification of hepatocarcinogen-resistance genes in DBA/2 mice	Genetics	139(1)	387-395	Jan	1995		http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7705639&dopt=Abstract	7705639	95220677	01	32 wks 	224		Male	11-40	number of tumors	1.6	0.5	31	4	2.7	0.9	14	2	22	2	1.3	0.4	18	3			63	3	1.7	0.4	8.2	3.6			0.06	0.04	22	2	16	2	43	3			14	2			5.8	1.2	15	2	12	2	14	3	5.6	1.0	2.3	0.6	3.5	1.0	8.6	1.3	8.1	1.5																							8/4/2003	MK Sullivan											7705639.01
Locomotor activity after 0.25 mg/kg of paraoxon from 1-5 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		03	7 wks	49		Male	3-10	activity counts/min	78.8	7.1	55.0	4.6	94.1	8.1	82.2	18.0	43.4	4.7	84.3	16.1	45.2	6.1			36.0	2.2	48.7	5.1	49.5	1.9	90.5	10.3	55.7	4.4	46.7	6.7	77.0	16.9	73.3	14.7			46.0	4.7					44.2	1.7	60.6	6.3	57.8	6.6	38.8	4.4	105.5	9.8	55.1	4.9	58.8	3.3	52.4	4.6																							7/13/2003	MK Sullivan	MK Sullivan										11106859.03
Locomotor activity after 10 ml/kg of oil from 1-5 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		04	7 wks	49		Male	3-10	activity counts/min	76.2	6.5	66.7	4.9	100.3	11.8	64.4	7.2	43.6	7.1	97.3	12.2	48.5	2.8			42.6	4.0	65.1	6.6	58.7	6.7	98.0	10.6	60.3	3.5	61.2	4.3	79.7	11.4	71.4	7.3			66.4	4.9					48.5	2.6	61.2	4.1	57.4	8.6	41.0	3.4	117.5	13.6	58.8	6.7	63.5	14.1	61.7	7.2																							7/13/2003	MK Sullivan	MK Sullivan										11106859.04
Locomotor activity after 0.25 mg/kg of paraoxon from 6-10 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		05	7 wks	49		Male	3-10	activity counts/min	26.2	7.1	13.2	2.5	29.3	4.0	41.8	10.5	15.9	1.3	43.1	5.1	26.4	4.4			19.8	4.0	20.6	5.3	8.1	1.3	33.8	3.4	17.6	4.8	12.6	2.6	34.5	11.3	25.8	7.2			16.2	3.9					6.1	2.1	25.2	3.3	27.4	6.0	11.3	2.7	42.9	6.1	29.5	5.9	14.2	1.5	9.2	1.6																							7/13/2003	MK Sullivan	MK Sullivan										11106859.05
Locomotor activity after 10 ml/kg of oil from 6-10 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		06	7 wks	49		Male	3-10	activity counts/min	45.3	5.4	50.6	4.3	64.1	12.6	35.3	10.2	24.0	6.1	60.7	7.8	35.5	7.7			25.9	3.1	39.9	2.0	33.6	5.6	42.7	3.7	29.3	5.0	36.5	4.3	42.0	7.0	51.0	4.5			44.2	2.1					27.1	3.3	47.3	3.6	34.2	5.1	26.5	5.0	61.4	12.5	30.1	5.6	38.8	4.6	40.1	7.2																							7/13/2003	MK Sullivan	MK Sullivan										11106859.06
Locomotor activity after 0.25 mg/kg of paraoxon from 11-15 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		07	7 wks	49		Male	3-10	activity counts/min	22.4	5.1	6.3	1.9	16.8	3.5	33.4	10.9	10.3	1.4	28.6	8.7	23.9	3.1			6.7	1.8	18.5	4.3	4.9	0.9	24.6	3.8	9.6	4.0	6.5	1.5	18.3	6.8	12.5	4.6			13.7	3.0					3.3	1.1	19.5	5.3	22.6	6.9	7.0	1.9	21.8	2.6	19.1	3.8	6.9	0.9	5.1	1.0																							7/13/2003	MK Sullivan	MK Sullivan										11106859.07
Locomotor activity after 10 ml/kg of oil from 11-15 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		08	7 wks	49		Male	3-10	activity counts/min	41.2	5.4	41.1	3.5	50.4	13.3	20.0	8.5	26.1	4.6	46.5	6.6	37.6	3.8			28.0	3.5	37.8	5.3	30.2	3.4	36.2	3.7	26.1	2.4	27.8	4.9	35.0	6.1	37.1	6.5			37.0	2.7					21.3	5.2	40.8	3.7	32.4	3.9	22.6	3.3	41.3	7.9	26.5	8.4	31.0	7.1	42.5	5.9																							7/13/2003	MK Sullivan	MK Sullivan										11106859.08
Locomotor activity after 0.25 mg/kg of paraoxon from 16-20 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		09	7 wks	49		Male	3-10	activity counts/min	17.6	3.8	3.8	1.1	10.7	2.4	29.7	11.0	4.9	0.7	25.7	11.7	18.6	3.3			10.6	5.8	15.6	6.0	2.5	1.4	21.1	6.0	7.6	4.3	6.8	2.9	20.9	9.6	8.4	2.4			10.9	2.3					0.8	0.5	17.2	7.2	16.5	6.9	6.4	2.3	15.0	3.9	21.1	4.5	3.7	1.3	2.0	0.6																							7/13/2003	MK Sullivan	MK Sullivan										11106859.09
Locomotor activity after 10 ml/kg of oil from 16-20 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		10	7 wks	49		Male	3-10	activity counts/min	42.7	3.9	42.8	5.8	53.2	10.4	22.4	7.9	19.4	6.0	36.4	8.1	31.7	4.0			29.6	4.0	33.6	4.3	29.3	3.5	37.6	2.8	26.7	2.1	18.9	2.8	29.3	6.7	33.8	5.6			36.4	3.8					17.5	6.3	32.5	3.8	29.4	3.5	20.9	5.5	42.5	9.7	23.3	6.5	30.9	4.7	36.2	4.7																							7/13/2003	MK Sullivan	MK Sullivan										11106859.1
Locomotor activity after 0.25 mg/kg of paraoxon from 21-25 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		11	7 wks	49		Male	3-10	activity counts/min	12.9	5.3	3.8	1.2	4.2	1.3	37.6	10.0	6.2	4.4	25.3	9.3	15.2	5.8			8.1	2.7	13.1	6.2	2.5	1.3	15.2	4.1	4.3	2.0	10.1	5.1	13.0	5.8	9.8	3.7			8.7	2.7					1.7	1.0	12.2	6.5	16.3	5.6	4.4	1.9	16.3	2.9	13.3	4.1	2.9	0.8	1.9	0.7																							7/13/2003	MK Sullivan	MK Sullivan										11106859.11
Locomotor activity after 10 ml/kg of oil from 21-25 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		12	7 wks	49		Male	3-10	activity counts/min	36.7	5.6	41.4	4.4	37.6	11.1	26.2	8.8	19.0	7.6	37.5	6.8	31.2	2.7			31.8	6.5	30.4	7.2	20.8	7.2	38.7	8.6	19.1	4.1	27.6	4.9	24.0	5.8	32.6	4.6			33.8	2.6					26.0	8.2	35.1	5.7	24.8	4.2	15.7	3.1	38.7	8.2	25.4	4.8	31.0	5.1	35.5	7.7																							7/13/2003	MK Sullivan	MK Sullivan										11106859.12
Locomotor activity after 0.25 mg/kg of paraoxon from 26-30 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		13	7 wks	49		Male	3-10	activity counts/min	16.2	6.0	3.2	1.4	2.6	1.4	30.6	8.1	5.3	3.5	27.0	8.6	16.4	3.4			8.4	2.6	5.6	1.7	0.7	0.6	17.2	5.2	5.0	2.2	7.7	3.2	24.0	10.3	6.6	2.0			6.9	2.9					3.5	2.0	13.1	6.8	19.1	5.0	6.9	2.6	17.9	3.2	12.1	3.7	3.6	2.3	2.3	0.6																							7/13/2003	MK Sullivan	MK Sullivan										11106859.13
Locomotor activity after 10 ml/kg of oil from 26-30 min [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		14	7 wks	49		Male	3-10	activity counts/min	38.3	4.6	34.8	4.9	38.2	8.8	30.6	12.0	29.8	10.0	36.6	4.2	32.1	2.8			27.6	3.6	29.1	3.1	17.0	7.4	41.2	4.9	25.6	5.6	17.7	3.7	23.6	4.0	40.4	5.5			27.2	5.9					11.0	2.8	28.4	5.1	21.2	3.8	17.4	4.5	33.8	7.7	23.5	8.5	25.8	5.0	33.2	6.6																							7/13/2003	MK Sullivan	MK Sullivan										11106859.14
Locomotor activity after 0.25 mg/kg of paraoxon in first 15 min of 30 min activity test [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		15	7 wks	49		Male	3-10	activity counts/min	43.1	4.92	25.3	2.05	48.1	4.01	52.8	11.91	23.6	1.20	53.0	5.85	32.6	4.13			21.8	1.94	29.3	4.96	21.7	0.85	50.8	4.80	28.6	4.04	22.4	2.65	43.7	10.20	37.6	7.96			25.1	2.97					18.2	1.07	35.7	2.89	36.8	5.85	19.5	2.13	57.9	5.85	34.7	3.94	27.3	0.74	22.6	2.01																							7/13/2003	MK Sullivan	MK Sullivan										11106859.15
Locomotor activity after 10 ml/kg of oil in first 15 min of 30 min activity test [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		16	7 wks	49		Male	3-10	activity counts/min	54.1	3.95	53.8	2.99	26.3	11.82	40.4	5.94	31.4	4.97	68.7	6.84	41.6	3.54			32.2	2.93	49.9	2.00	41.8	4.92	60.0	5.80	39.6	1.69	42.5	2.85	52.7	3.67	53.9	5.91			49.8	2.94					32.2	1.90	50.6	2.79	41.5	5.16	30.4	3.67	73.7	10.73	38.6	6.93	44.3	7.01	48.8	4.93																							7/13/2003	MK Sullivan	MK Sullivan										11106859.16
Locomotor activity after 0.25 mg/kg of paraoxon in last 15 min of 30 min activity test  [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		17	7 wks	49		Male	3-10	activity counts/min	16.3	3.90	4.3	0.87	6.3	0.85	33.5	8.94	5.7	1.13	26.0	10.15	17.6	4.04			9.5	4.04	11.4	4.18	2.5	0.33	18.9	4.92	6.3	2.00	8.5	4.04	19.5	7.59	8.4	1.92			9.4	2.24					2.5	1.08	14.5	6.92	17.3	5.26	6.2	1.92	16.4	3.02	15.5	4.24	3.7	1.12	2.26	0.68																							7/13/2003	MK Sullivan	MK Sullivan										11106859.17
Locomotor activity after after 10 ml/kg of oil in last 15 min of 30 min activity test [activity counts/min]		Genetic mechanisms responsible for organophosphate (OP)-induced behavioral changes remain obscure. In the present study, provisional quantitative trait loci (QTL) associated with acute sensitivity or insensitivity to hypolocomotion produced by the OP paraoxon were identified. Naive adult male and female mice of the BXD/Ty series (22 different BXD strains plus C57BL/6J and DBA/2J progenitor strains) received 0 or 0.25 mg/kg paraoxon (IP), immediately before placement in an activity chamber for a 30-min test. As expected, based on dose-response and time course studies with Swiss-Webster, C57BL/6, and DBA/2 mice, paraoxon treatment reduced locomotor activity in most, but not all BXD strains. Heritability (proportion of phenotypic variability attributed to genetic differences) was 0. 58 for the paraoxon treatment effect. Difference scores (strain mean for vehicle activity minus strain mean for paraoxon activity), and percent change in activity of paraoxon-treated mice compared to vehicle-treated mice were calculated for each BXD strain. QTL analyses using activity difference scores and percentage change in activity were conducted using a database with over 1300 unique genetic markers. Several provisional QTL found on different chromosomes were associated with the activity phenotype. Of these, several markers attained p<0.01 or greater. These were as follows: Chr 1: Ly9, p<0.006; Chr 6: D6Ncvs44, p<0.0005; Chr 9: D9Mit15, p<0. 003; Chr 11: D11Ncvs76, p<0.002; Chr 15: Tstap198, p<0.008. In addition, several markers on chromosome 3 approached p<0.01. Identified genes found near these regions include two plasma carboxylesterase alleles on chromosomes 6 and 9, a glutamate receptor subtype on chromosome 11 and a glycine receptor subunit on chromosome 11, raising the possibility that these genes could be the basis for these provisional QTLs.	Risinger FO, Quick E, Belknap JK	Quantitative trait loci for acute behavioral sensitivity to paraoxon	Neurotoxicol Teratol	22(5)	667-674	Sep-Oct	2000		http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11106859&dopt=Abstract	11106859		18	7 wks	49		Male	3-10	activity counts/min	40.0	4.21	40.8	5.08	43.6	10.1	26.0	8.23	23.7	7.79	37.4	6.27	32.4	3.17			30.4	4.23	31.0	4.55	22.3	5.91	39.5	5.11	24.7	2.64	21.4	2.15	26.4	5.25	26.1	5.58			32.9	2.70					18.2	4.13	32.7	4.33	25.3	3.31	18.3	4.17	38.4	8.37	24.6	5.87	29.7	4.22	35.7	5.12																							7/13/2003	MK Sullivan	MK Sullivan										11106859.18