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Mecamylamine and Ethanol Preference in Healthy Volunteers
Author(s) -
Young Elizabeth M.,
Mahler Stephen,
Chi Henry,
Wit Harriet
Publication year - 2005
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1097/01.alc.0000150007.34702.16
Subject(s) - mecamylamine , alcohol , nicotinic agonist , ethanol , psychology , craving , placebo , pharmacology , nicotinic antagonist , anhedonia , medicine , addiction , psychiatry , receptor , chemistry , biochemistry , schizophrenia (object oriented programming) , alternative medicine , pathology
Background: Recent evidence suggests that some of the behavioral effects of alcohol may be mediated through actions on nicotinic acetylcholine receptors. Mecamylamine, a nicotinic acetylcholine receptor antagonist, reduces alcohol preference and consumption in alcohol‐preferring rats, and in humans, mecamylamine dampens some of the subjective, or mood‐altering, effects of alcohol. This experiment was designed to investigate the effects of mecamylamine on consumption of alcohol in healthy social drinkers. Methods: Healthy volunteers (12 men, 12 women) participated in a choice procedure in which they chose between an alcoholic beverage and money (low, medium, or high amounts) after pretreatment with mecamylamine (7.5 or 15 mg) or placebo. Outcome measures were the number of alcoholic beverages consumed and the subjective effects of alcohol. Results: Mecamylamine (15 mg) decreased blood alcohol levels (BALs) after a small fixed dose of alcohol (0.2 g/kg). Even when the lower BALs were taken into account, mecamylamine reduced ratings of stimulation after alcohol (Addiction Research Center Inventory A scale). Mecamylamine did not significantly reduce choice for alcohol versus money. However, there was a tendency for the drug to decrease alcohol choice among participants who reported the greatest stimulant‐like effects from alcohol. Conclusion: These results provide only limited support for the idea that nicotinic acetylcholine receptors are involved in the rewarding effects of alcohol.