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.
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.
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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