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枪乌贼巨大轴突中的门控电流与钾通道

Gating current and potassium channels in the giant axon of the squid.

作者信息

Gilly W F, Armstrong C M

出版信息

Biophys J. 1980 Mar;29(3):485-92. doi: 10.1016/S0006-3495(80)85147-2.

Abstract

Gating current (Ig) underlying Na-channel activation is large enough to enable resolution of components both preceding and paralleling Na conductance (gNa) turn-on. For large depolarizations (beyond +20 mV), an additional "slow phase" of Ig is observed during a time when Na activation is already complete, but when K-channel opening is just becoming detectable. If Na- and K-channel gating are similar, the slow kinetics and long delay for K activation predict that K channel Ig must be relatively small and slow. Externally applied dibucaine almost totally blocks gNa and greatly reduces the fast (Na channel) Ig without altering gK or the Ig slow phase. The slow phase of Ig depends in part of the presence of functional K channels. Selective diminution in amplitude of the slow phase is consistently observed after a 30-min perfusion with both external and internal K-free media, a procedure which destroys nearly all K channels. This decrease of Ig amounts to approximately 10% of the total charge movements at +40 to +80 mV, with gating charge and K channels disappearing in a ratio of less than 1 e- per picosiemens of gK. These findings are consistent with the idea that part of the Ig slow phase represents gating current generated by the early steps in K-channel activation.

摘要

钠通道激活所产生的门控电流(Ig)足够大,能够分辨出在钠电导(gNa)开启之前和平行阶段的各个成分。对于较大的去极化(超过+20 mV),在钠激活已经完成但钾通道开放刚刚开始可检测到时,会观察到Ig的一个额外“慢相”。如果钠通道和钾通道的门控相似,钾激活的慢动力学和长延迟表明钾通道Ig必定相对较小且缓慢。外部施加的丁卡因几乎完全阻断gNa,并极大地降低快速(钠通道)Ig,而不改变gK或Ig慢相。Ig的慢相部分取决于功能性钾通道的存在。在用外部和内部无钾培养基灌注30分钟后,始终观察到慢相幅度的选择性减小,该过程几乎破坏了所有钾通道。在+40至+80 mV时,Ig的这种减少量约占总电荷移动的10%,门控电荷与钾通道以小于每皮西门子gK 1个电子的比例消失。这些发现与Ig慢相部分代表钾通道激活早期步骤产生的门控电流这一观点一致。

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A gating signal for the potassium channel?
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