Ethanol Modulation of Nicotinic Acetylcholine Receptor Currents in Cultured Cortical Neurons

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Vol. 55, Issue 1, 39-49, January 1999

Ethanol Modulation of Nicotinic Acetylcholine Receptor Currents in Cultured Cortical Neurons

Gary L. Aistrup, William Marszalec, and Toshio Narahashi

Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, Chicago, Illinois

Ethanol, at physiologically relevant concentrations, significantly enhanced high-affinity neuronal nicotinic acetylcholinereceptor (NnAChR) currents insensitive to $alpha$ -bungarotoxin ( $alpha$ -BuTX-ICs)in cultured rat cortical neurons in a fast and reversible manner,as determined by standard whole-cell patch-clamp recording techniques.The enhancement was (mean ± S.D.) 7.7 ± 5% to 192 ± 52% upon coapplicationof 3 to 300 mM ethanol with 1 to 3 µM ACh. No plateau for thisethanol-induced enhancement of $alpha$ -BuTX-ICs was reached. The maximal $alpha$ -BuTX-IC evoked by very high concentrations of ACh also was increasedupon coapplication of ethanol. In contrast, ethanol weakly inhibitedlow-affinity NnAChR currents sensitive to $alpha$ -BuTX ( $alpha$ -BuTX-SCs)(5 ± 4% to 29 ± 6% inhibition by 10 to 300 mM ethanol at 300 to1000 µM ACh). This neuronal preparation also enabled comparisonof ethanol action on NnAChRs with its action on N-methyl-D-aspartatereceptor currents and $gamma$ -aminobutyric acid receptor currents withinthe same neurons. Ethanol (100 mM) was more potent at enhancingNnAChR $alpha$ -BuTX-ICs (61 ± 9% enhancement) than it was at enhancing $gamma$ -aminobutyric acid receptor current (3 ± 3% enhancement $---$ not statisticallysignificant) or at inhibiting N-methyl-D-aspartate receptor currents(~35 ± 7% inhibition). Thus, NnAChRs, particularly those insensitiveto $alpha$ -BuTX, may be sensitive conduits through which ethanol canmediate some of its actions in thebrain.

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