GLUCOSE, SULFONYLUREAS, AND NEUROTRANSMITTER RELEASE - ROLE OF ATP-SENSITIVE K+ CHANNELS
GLUCOSE, SULFONYLUREAS, AND NEUROTRANSMITTER RELEASE - ROLE OF ATP-SENSITIVE K+ CHANNELS
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DOI：
10.1126/science.2305257
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发表时间：
1990-02-16
期刊：
影响因子：
56.9
通讯作者：
LAZDUNSKI, M
中科院分区：
文献类型：
--
作者：
AMOROSO, S;SCHMIDANTOMARCHI, H;LAZDUNSKI, M
磺酰脲敏感性三磷酸腺苷（ATP）调节钾（KATP）通道存在于脑细胞中，并在神经末梢的神经分泌中发挥作用。黑质（一个显示出高磺酰脲结合的脑区）中的KATP通道被高葡萄糖浓度和抗糖尿病磺酰脲灭活，并被ATP耗竭和缺氧激活。KATP通道抑制导致γ-ATP的激活。氨基丁酸（GABA）释放，而KATP通道激活导致GABA释放的抑制。这些通道可能参与大脑对高血糖和低血糖（糖尿病）以及缺血或缺氧的反应。
Sulfonylurea-sensitive adenosine triphosphate (ATP)-regulated potassium (KATP) channels are present in brain cells and play a role in neurosecretion at nerve terminals. KATP channels in substantia nigra, a brain region that shows high sulfonylurea binding, are inactivated by high glucose concentrations and by antidiabetic sulfonylureas and are activated by ATP depletion and anoxia. KATP channel inhibition leads to activation of .gamma.-aminobutyric acid (GABA) release, whereas KATP channel activation leads to inhibition of GABA release. These channels may be involved in the response of the brain to hyper- and hypoglycemia (in diabetes) and ischemia or anoxia.