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KCNQ2和KCNQ3钾通道亚基:M通道的分子关联

KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel.

作者信息

Wang H S, Pan Z, Shi W, Brown B S, Wymore R S, Cohen I S, Dixon J E, McKinnon D

机构信息

Institute of Molecular Cardiology, Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.

出版信息

Science. 1998 Dec 4;282(5395):1890-3. doi: 10.1126/science.282.5395.1890.

DOI:10.1126/science.282.5395.1890
PMID:9836639
Abstract

The M-current regulates the subthreshold electrical excitability of many neurons, determining their firing properties and responsiveness to synaptic input. To date, however, the genes that encode subunits of this important channel have not been identified. The biophysical properties, sensitivity to pharmacological blockade, and expression pattern of the KCNQ2 and KCNQ3 potassium channels were determined. It is concluded that both these subunits contribute to the native M-current.

摘要

M电流调节许多神经元的阈下电兴奋性,决定其放电特性和对突触输入的反应性。然而,迄今为止,编码这一重要通道亚基的基因尚未被鉴定出来。研究确定了KCNQ2和KCNQ3钾通道的生物物理特性、对药理学阻断的敏感性及表达模式。得出的结论是,这两个亚基均对天然M电流有贡献。

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KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel.KCNQ2和KCNQ3钾通道亚基:M通道的分子关联
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Activation of expressed KCNQ potassium currents and native neuronal M-type potassium currents by the anti-convulsant drug retigabine.抗惊厥药物瑞替加滨对表达的KCNQ钾电流和天然神经元M型钾电流的激活作用。
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Benign familial neonatal convulsions caused by altered gating of KCNQ2/KCNQ3 potassium channels.由KCNQ2/KCNQ3钾通道门控改变引起的良性家族性新生儿惊厥。
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Differential expression of kcnq2 splice variants: implications to m current function during neuronal development.KCNQ2剪接变体的差异表达:对神经元发育过程中M电流功能的影响。
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Nature. 1998 Dec 17;396(6712):687-90. doi: 10.1038/25367.

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