Modulating anxiety and activity.
Modulating anxiety and activity.
复制标题
调节焦虑和活动。
DOI：
10.1126/science.aaz3176
复制
发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Moss,StephenJ
中科院分区：
文献类型：
--
作者：
Rudolph,Uwe;Moss,StephenJ
中枢神经系统的快速突触抑制是由抑制性神经递质γ-氨基丁酸（GABA） A型（GABAA）受体实现的。这些受体是突触后五聚体复合物，形成一个可渗透氯离子的中心孔。GABA通常会增加氯离子的流入，导致突触后膜的超极化，使其不易兴奋。gaba受体调节警觉性、情绪、认知和肌肉紧张，它们是减少焦虑和镇静催眠的苯二氮卓类药物和一些全身麻醉剂（如异丙酚）的目标。这些药物增加gaba诱导的氯离子电流(1)。在本期的第246页，Hanet al.(2)描述了一种与gaba受体相互作用并调节其对苯二氮卓类药物反应的辅助蛋白的鉴定。这些发现对理解苯二氮卓类药物的作用具有相当大的意义，因为它们重新定义了支持其作用所需的最低成分。
Fast synaptic inhibition in the central nervous system is achieved by the inhibitory neurotransmitter γ-aminobutyric acid (GABA) type A (GABAA) receptors. These receptors are postsynaptic pentameric complexes that form a central pore that is permeable to chloride ions. GABA typically increases chloride influx, which results in hyperpolarization of the postsynaptic membrane, rendering it less excitable. GABAAreceptors modulate vigilance, emotions, cognition, and muscle tension, and they are the targets of anxiety-reducing and sedative-hypnotic benzodiazepines and some general anesthetics, such as propofol. These drugs increase GABA-induced chloride currents (1). On page 246 of this issue, Hanet al.(2) describe the identification of an auxiliary protein that interacts with GABAAreceptors and modulates their response to benzodiazepines. These findings have considerable implications for understanding benzodiazepine action because they redefine the components minimally required to support their actions.