Potentiation of γ‐Aminobutyric Acid‐Mediated Chloride Flux by Pentobarbital and Diazepam but Not Ethanol

Abstract

The influx of ³⁶Cl^‐ into cerebral cortical and cerebellar microsacs from ICR mice and Sprague‐Dawley rats was studied in incubations lasting 3 s, 500 ms, or 21 ms. In the 3‐s assay, 10‐40 mM ethanol did not affect either basal or γ‐arninobutyric acid (GABA)‐mediated Cl^‐ flux, at any GABA concentration tested. Only at a concentration of 600 mM did ethanol potentiate Cl^‐ flux in both mouse and rat preparations. Ethanol (20 mM) also did not affect the significant potentiation of GABA‐mediated flux produced by 50 γM pentobarbital or 2 γM diazepam in ICR mouse microsacs. In 21‐ and 500‐ms incubations (quench‐flow method), 50 γM pentobarbital significantly potentiated GABA‐mediated Cl^‐ flux in rat cortical microsacs, but 10‐50 mM ethanol did not. These studies suggest that some as yet unrecognized factor is essential for ethanol enhancement of GABA‐mediated Cl^‐ flux, as reported by others in brain homogenates and in tissue culture.