Citation

Suzdak PD, Schwartz RD, Skolnick P, Paul SM. Brain Res. 1988; 444(2): 340-345.

Affiliation

Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892.

Copyright

(Copyright © 1988, International Brain Research Organization, Publisher Elsevier Publishing)

DOI

unavailable

PMID

2834024

Abstract

A series of short-chain alcohols, including ethanol, were examined for their abilities to stimulate gamma-aminobutyric acid (GABA) receptor-mediated chloride uptake into isolated brain vesicles. All of the alcohols tested stimulated 36 chloride uptake, at concentrations that occur during acute intoxication, and their potencies in stimulating GABA receptor-mediated chloride uptake were highly correlated with both their intoxication potencies in rats (r = 0.96; P less than 0.0001) and their membrane/buffer partition coefficients (r = 0.91; P less than 0.0005). Thus, the activity of alcohols at the GABA receptor-coupled chloride ion channel appears to be related to their ability to enter hydrophobic regions of the neuronal membrane. These data suggest that the anxiolytic, sedative/hypnotic and intoxicating properties of ethanol may, in part, be mediated via an action at central GABA receptors.

Language: en