Barker J L, McBurney R N
Proc R Soc Lond B Biol Sci. 1979 Dec 31;206(1164):319-27. doi: 10.1098/rspb.1979.0108.
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.
抗惊厥巴比妥酸盐苯巴比妥可增加培养的小鼠脊髓神经元对γ-氨基丁酸（GABA）的膜电流和电导反应。对对照条件下及存在苯巴比妥时GABA电流波动的分析表明，其主要作用是增加GABA激活通道保持开放的平均时间。该药物可延长衰减时间常数与GABA激活通道平均开放时间相似的微小突触电流的持续时间。结果表明：（1）突触事件是由GABA介导的；（2）巴比妥酸盐对这些事件的增强作用是由于该药物的突触后作用。
