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四甲铵离子改变黏液虫中的钠通道门控。

Tetramethylammonium ions alter sodium-channel gating in Myxicola.

作者信息

Schauf C L

出版信息

Biophys J. 1983 Mar;41(3):269-74. doi: 10.1016/S0006-3495(83)84437-3.

Abstract

In Myxicola axons, substitution of tetramethylammonium (TMA+) for Cs+ alters intramembrane charge movements (gating currents). Although the total charge moved during and following a depolarizing step remains constant, with TMA+ the ON response has additional slower component(s), and the OFF response is retarded. Concommitantly, TMA+ produces the same voltage-dependent block of Na+ inactivation in Myxicola as has been observed in other preparations. At large positive potentials as many as 70% of the Na+ channels fail to inactivate in the steady state. In addition, TMA+ slows Na+ activation, retards the inactivation of those Na+ channels that remain able to inactivate, and decreases the maximum Na+ conductance. The steady-state Na+ conductance induced by internal TMA+ or Na+ is consistent with a scheme in which these internal cations simply modify Na+ channels in an all-or-none fashion so that a fraction become incapable of inactivating.

摘要

在黏液虫轴突中,用四甲基铵(TMA⁺)替代Cs⁺会改变膜内电荷移动(门控电流)。尽管在去极化步骤期间及之后移动的总电荷量保持不变,但使用TMA⁺时,开启响应有额外的较慢成分,且关闭响应延迟。同时,TMA⁺在黏液虫中产生与其他制剂中观察到的相同的电压依赖性Na⁺失活阻断。在大的正电位下,多达70%的Na⁺通道在稳态下无法失活。此外,TMA⁺减缓Na⁺激活,延迟那些仍能失活的Na⁺通道的失活,并降低最大Na⁺电导。由内部TMA⁺或Na⁺诱导的稳态Na⁺电导与这样一种机制一致,即这些内部阳离子简单地以全或无的方式修饰Na⁺通道,使得一部分通道变得无法失活。

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