Localization of genes affecting alcohol drinking in mice.
paper
Cited
Public
Unavailable
- Authors
- Phillips, T J; Crabbe, J C; Metten, P; Belknap, J K
- Year
- 1994
- Journal
- Alcoholism, clinical and experimental research
- PMID
- 7978106
- DOI
- 10.1111/j.1530-0277.1994.tb00062.x
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.
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| Genetics and behavioral medicine. | McClearn GE et al. | β | 1996 | β |
| Identification of sex-specific quantitative trait loci controlling alcohol preference in C57BL/ 6 mice. | Melo JA et al. | β | 1996 | β |
| Inbred mouse strains vary in oral self-selection of nicotine. | Robinson SF et al. | β | 1996 | β |
| Intake of ethanol, sodium chloride, sucrose, citric acid, and quinine hydrochloride solutions by mice: a genetic analysis. | Bachmanov AA et al. | β | 1996 | β |
| No association of the structural dopamine D2 receptor (DRD2) variant 311Cys with alcoholism. | Finckh U et al. | β | 1996 | β |
| Quantitative trait locus analyses of sleep-times induced by sedative-hypnotics in LSXSS recombinant inbred strains of mice. | Christensen SC et al. | β | 1996 | β |
| Quantitative trait locus gene mapping: a new method for locating alcohol response genes. | Crabbe JC | β | 1996 | β |
| Self-administration of ethanol: towards the location of predisposing polygenes in quasi-congenic animal models. | VadΓ‘sz C et al. | β | 1996 | β |
| The biological, social and clinical bases of drug addiction: commentary and debate. | Altman J et al. | β | 1996 | β |
| Type I and type II error rates for quantitative trait loci (QTL) mapping studies using recombinant inbred mouse strains. | Belknap JK et al. | β | 1996 | β |
| Voluntary alcohol consumption in BXD recombinant inbred mice: relationship to alcohol metabolism. | Gill K et al. | β | 1996 | β |
| Effects of acute and repeated ethanol exposures on the locomotor activity of BXD recombinant inbred mice. | Phillips TJ et al. | β | 1995 | β |
| Localization of genes influencing ethanol-induced conditioned place preference and locomotor activity in BXD recombinant inbred mice. | Cunningham CL | β | 1995 | β |
| Genetic animal models of alcohol and drug abuse. | Crabbe JC et al. | β | 1994 | β |