Phenobarbitone modulation of postsynaptic GABA receptor function on cultured mammalian neurons

Abstract

The anticonvulsant barbiturate phenobarbitone increases membrane current and conductance responses to gamma-aminobutyric acid (GABA) in cultured mouse spinal neurons. Analyses of GABA current fluctuations under control conditions and in the presence of phenobarbitone show that the principle action is to increase the average time during which GABA-activated channels remain open. The duration of minature synaptic currents with a time constant of decay similar to the mean open-time of GABA-activated channels is prolonged by the drug. The results suggest that (1) the synaptic events are GABA-mediated and (2) the enhancement of these events by barbiturate is due to the postsynaptic action of the drug.