Alcohol modulation of cloned GABAA receptor-channel complex expressed in human kidney cell lines.

The effects of n-octanol on GABA-induced currents were examined on the alpha 1 beta 2 gamma 2s and alpha 1 beta 2 combinations of GABAA receptor subunits expressed in a human kidney cell line (HEK 293), using the whole-cell variation of the patch clamp technique. The EC50 of the GABA dose-response curve for the alpha 1 beta 2 combination was lower than that for the alpha 1 beta 2 gamma 2s combination. n-Octanol at 100 microM augmented the GABA-induced currents in a dose-dependent manner, decreasing the EC50 of the GABA dose-response curve without affecting the maximal response. The magnitude of n-octanol potentiation was nearly the same in both combinations. In contrast, a benzodiazepine agonist, chlordiazepoxide, augmented the currents of the alpha 1 beta 2 gamma 2s combination only. We conclude that the potentiation of GABAA receptor-mediated currents by a long carbon chain n-alcohol does not require the gamma 2 subunit.