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Potentiation of γ‐Aminobutyric Acid‐Mediated Chloride Flux by Pentobarbital and Diazepam but Not Ethanol
Author(s) -
Mihic S. J.,
Wu P. H.,
Kalant H.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb09781.x
Subject(s) - pentobarbital , ethanol , long term potentiation , chemistry , diazepam , medicine , endocrinology , aminobutyric acid , biophysics , biochemistry , pharmacology , biology , receptor
The influx of 36 Cl ‐ 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 m M 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 m M did ethanol potentiate Cl ‐ flux in both mouse and rat preparations. Ethanol (20 m M ) 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 m M 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.