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树眼镜蛇毒素可阻断钾通道,并减缓黏液虫巨型轴突中的钠失活。

Dendrotoxin blocks potassium channels and slows sodium inactivation in Myxicola giant axons.

作者信息

Schauf C L

出版信息

J Pharmacol Exp Ther. 1987 Jun;241(3):793-6.

PMID:2439682
Abstract

Dendrotoxin (DTX) is known to partially block delayed rectifier K+ channels and enhance neurotransmitter release, but no effects on Na+ channels have been reported. In voltage-clamped Myxicola axons DTX affected both the K+ and Na+ conductances. DTX blocked completely Myxicola K+ channels with a KD of 150 nM and induced slow K+ inactivation. DTX doubled the time constants for inactivation of conducting Na+ channels and gating charge immobilization without altering Na+ activation or the voltage- and time-dependent fast and slow Na+ inactivation induced by depolarizing prepulses. A selective effect on open Na+ channel inactivation provides additional evidence for kinetic models in which resting Na+ channels need not open before being inactivated.

摘要

已知树眼镜蛇毒素(DTX)可部分阻断延迟整流钾通道并增强神经递质释放,但尚未有其对钠通道影响的报道。在电压钳制的粘液虫轴突中,DTX对钾电导和钠电导均有影响。DTX以150 nM的解离常数完全阻断粘液虫钾通道,并诱导缓慢的钾失活。DTX使传导性钠通道失活和门控电荷固定的时间常数增加一倍,而不会改变钠激活或由去极化预脉冲诱导的电压和时间依赖性快速和缓慢钠失活。对开放钠通道失活的选择性作用为动力学模型提供了额外证据,在该模型中,静息钠通道在失活前无需开放。

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