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Abstract
Sensitivity to ethanol’s stimulant effects may increase risk for alcohol use disorders. FAST and SLOW mouse lines differ in this sensitivity and in muscarinic acetylcholine receptor function. Behavioral and genetic studies revealed that muscarinic antagonism in the nucleus accumbens does not explain prior synergistic effects with ethanol. FAST mice showed higher Chrm5 expression, and knockout studies confirmed the m5 receptor is required for ethanol-induced stimulation, while m4 had no effect. Neither receptor influenced ethanol consumption. These findings implicate Chrm5 as a key contributor to ethanol sensitivity, while Chrm4 is unlikely to play a role.