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Elevated alcohol consumption in null mutant mice lacking 5-HT1B serotonin receptors
J C Crabbe1, T J Phillips, D J Feller
1Department of Veterans, Affairs Medical Center, Portland, Oregon, USA.
Nature Genetics
|September 1, 1996
Summary
Mice lacking the serotonin 5-HT1B receptor gene drank more alcohol and showed reduced sensitivity to its ataxic effects. This suggests the serotonin 5-HT1B receptor influences alcohol consumption and response.
Area of Science:
- Neuroscience
- Pharmacology
- Genetics
Background:
- Alcohol consumption is linked to serotonin (5-HT) functioning.
- Lowered 5-HT neurotransmission is observed in some alcoholics, potentially correlating with aggression.
- Serotonin systems impact ethanol sensitivity and tolerance in rodents.
Purpose of the Study:
- To investigate the role of the serotonin 5-HT1B receptor in alcohol drinking and sensitivity.
- To characterize the behavior of mice lacking the 5-HT1B receptor gene (5-HT1B-/-) in response to ethanol.
Main Methods:
- Utilized 5-HT1B-/- mutant mice and wild-type littermates.
- Assessed voluntary ethanol consumption, including preference for ethanol solutions.
- Evaluated sensitivity to ethanol-induced ataxia, tolerance development, withdrawal, and metabolism.
Main Results:
- 5-HT1B-/- mice consumed twice as much ethanol as wild-type mice.
- Mutant mice exhibited reduced sensitivity to ethanol-induced ataxia and slower tolerance development.
- No significant differences were observed in ethanol withdrawal or metabolism between genotypes.
Conclusions:
- The serotonin 5-HT1B receptor plays a role in regulating ethanol intake.
- Serotonergic system manipulation can alter ethanol's ataxic effects without impacting dependence.
