GABA-activated chloride channels in secretory nerve endings.
GABA-activated chloride channels in secretory nerve endings.
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分泌神经末梢中 GABA 激活的氯离子通道。
DOI：
10.1126/science.8380942
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Jackson,MB
中科院分区：
文献类型：
--
作者：
Zhang,SJ;Jackson,MB
作用于突触前终末的神经递质调节突触的传递和可塑性。由于直接从小型突触前终末进行电生理记录的困难，人们对介导这些活动的离子通道或改变递质分泌的机制知之甚少。膜片钳技术显示，突触前神经递质γ-氨基丁酸(GABA)激活GABA受体，并在垂体后叶多肽能神经末梢膜上开启氯离子通道。GABA开放氯离子通道使神经末梢膜弱去极化，阻断动作电位。通过这种方式，GABA通过延缓兴奋进入末端分枝的扩散来限制分泌。
Neurotransmitters acting on presynaptic terminals regulate synaptic transmission and plasticity. Because of the difficulty of direct electrophysiological recording from small presynaptic terminals, little is known about the ion channels that mediate these actions or about the mechanisms by which transmitter secretion is altered. The patch-clamp technique is used to show that the predominant inhibitory presynaptic neurotransmitter, γ-aminobutyric acid (GABA), activates a GABAAreceptor and gates a chloride channel in the membranes of peptidergic nerve terminals of the posterior pituitary. The opening of a chloride channel by GABA weakly depolarizes the nerve terminal membrane and blocks action potentials. In this way, GABA limits secretion by retarding the spread of excitation into the terminal arborization.