Eghbali M, Curmi J P, Birnir B, Gage P W
John Curtin School of Medical Research, Australian National University, Canberra.
Nature. 1997 Jul 3;388(6637):71-5. doi: 10.1038/40404.
Benzodiazepines, which are widely used clinically for relief of anxiety and for sedation, are thought to enhance synaptic inhibition in the central nervous system by increasing the open probability of chloride channels activated by the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Here we show that the benzodiazepine diazepam can also increase the conductance of GABAA channels activated by low concentrations of GABA (0.5 or 5 microM) in rat cultured hippocampal neurons. Before exposure to diazepam, chloride channels activated by GABA had conductances of 8 to 53pS. Diazepam caused a concentration-dependent and reversible increase in the conductance of these channels towards a maximum conductance of 70-80 pS and the effect was as great as 7-fold in channels of lowest initial conductance. Increasing the conductance of GABAA channels tonically activated by low ambient concentrations of GABA in the extracellular environment may be an important way in which these drugs depress excitation in the central nervous system. That any drug has such a large effect on single channel conductance has not been reported previously and has implications for models of channel structure and conductance.
苯二氮䓬类药物在临床上广泛用于缓解焦虑和镇静,据认为它们通过增加由抑制性神经递质γ-氨基丁酸(GABA)激活的氯离子通道的开放概率来增强中枢神经系统中的突触抑制作用。在此我们表明,苯二氮䓬类药物地西泮还可增加大鼠培养海马神经元中由低浓度GABA(0.5或5微摩尔)激活的GABAA通道的电导。在暴露于地西泮之前,由GABA激活的氯离子通道的电导为8至53皮西门子。地西泮导致这些通道的电导呈浓度依赖性且可逆地增加,最大电导达到70 - 80皮西门子,对于初始电导最低的通道,这种效应高达7倍。增加细胞外环境中由低环境浓度GABA持续激活的GABAA通道的电导,可能是这些药物抑制中枢神经系统兴奋的一种重要方式。此前尚未报道过任何药物对单通道电导有如此大的影响,这对通道结构和电导模型具有重要意义。