Alterations in γ‐Aminobutyric Acid Receptor Sensitivity Following Acute and Chronic Ethanol Treatments

Abstract

Abstract: The effects of acute and chronic ethanol ingestion on the binding of the inhibitory neurotransmitter 3 H‐γ‐aminobutyric acid (GABA) was investigated in inbred strains of mice. Acute effects were analyzed in DBA/2J (alcohol avoiding) and C57BL/6J (alcohol preferring) mice, while chronic effects were analyzed in C57 mice. Acute ethanol (4 g/kg) produced a significant increase in the binding capacity of the low‐affinity γ‐aminobutyric acid binding site in both C57 (12%) and DBA (23%) mice, without significantly altering other binding parameters. The enhanced binding capacity may be responsible for the behavioral depression associated with ethanol use. Chronically treated C57 mice exhibited a decrease in the density of low‐affinity GABA receptor sites. These results suggest the possible involvement of γ‐aminobutyric acid synaptic function in the neuropharmacological effects of ethanol. The possibility that chronic ethanol administration may result in adaptation of γ‐aminobutyric acid receptors to the continuous presence of ethanol‐induced central nervous system depression is discussed.