Excitation of rat cerebellar Golgi cells by ethanol: further characterization of the mechanism.

Background Studies with rodents suggest that acute ethanol exposure impairs information flow through the cerebellar cortex, in part, by increasing GABAergic input to granule cells. Experiments suggest that an increase in the excitability of specialized GABAergic interneurons that regulate granule cell activity (i.e. Golgi cells, GoCs) contributes to this effect. In GoCs, ethanol increases spontaneous action potential firing frequency, decreased the afterhyperpolarization amplitude, and depolarized the membrane potential. Studies suggest that these effects could be mediated by inhibition of the Na+/K+ ATPase. The purpose of this study was to characterize the potential role of other GoC conductances in the mechanism of action of ethanol.