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

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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.