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Biochem Pharmacol. 2004 Oct 15;68(8):1515-25.

A role for GABA mechanisms in the motivational effects of alcohol.

Author information

1
Department of Neuropharmacology, The Scripps Research Institute, 1055 North Pines Road, La Jolla, CA 92037, USA. gkoob@scripps.edu

Abstract

Low doses of ethanol have been hypothesized to act directly via proteins that form ligand-gated receptor channels, such as the gamma-aminobutyric acid (GABA) receptor complex, to allosterically alter function, particularly in specific brain areas such as those hypothesized to be involved in ethanol reinforcement. At the pharmacological level, one can antagonize the effects of ethanol with GABA antagonists, particularly its sedative, anxiolytic-like and acute reinforcing actions. Brain sites involved in the GABAergic component of ethanol reinforcement include the ventral tegmental area, elements of the extended amygdala (including the central nucleus of the amygdala), and the globus pallidus. Chronic administration of ethanol sufficient to produce dependence and increased ethanol intake are associated with increased GABA release in the amygdala and increased sensitivity to GABA agonists. A hypothesis is proposed that GABAergic interactions with the brain stress neurotransmitter corticotropin-releasing factor in specific elements of the extended amygdala may be an important component for the motivation for excessive drinking associated with the transition from social drinking to addiction.

Republished in

PMID:
15451394
DOI:
10.1016/j.bcp.2004.07.031
[Indexed for MEDLINE]

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