Sodium-activated potassium channels are functionally coupled to persistent sodium currents.
Sodium-activated potassium channels are functionally coupled to persistent sodium currents.
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DOI：
10.1523/jneurosci.5088-11.2012
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发表时间：
2012-02-22
期刊：
影响因子：
--
通讯作者：
Salkoff L
中科院分区：
文献类型：
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作者：
Hage TA;Salkoff L
我们报道了一种新的钠活化钾电流（IKNa）和持续钠电流（INaP）耦合系统，其组分广泛分布于整个大脑。它的存在和重要性以前没有被认识到。虽然已知IKNa存在于许多类型的细胞中，但激活IKNa的Na+的来源仍然是一个谜。我们现在发现，在大鼠神经元胞体产生的单个膜斑块中，钠通过INaP流入足以激活KNa通道，而不需要瞬态钠电流或大量[Na+]i的实质性贡献。INaP在细胞膜静息电位下被发现是活跃的，这一发现可能解释了为什么IKNa可以从负持有电位中被唤起。这些结果表明，INaP在激活负反馈系统以对抗INaP的兴奋效应方面具有意想不到的作用；INaP和IKNa的相互关系提示了神经元调节其兴奋性的新方法。
We report a novel coupled system of sodium-activated potassium currents (IKNa) and persistent sodium currents (INaP), the components of which are widely distributed throughout the brain. Its existence and importance has not been previously recognized. Although IKNa was known to exist in many cell types, the source of Na+ which activates IKNa remained a mystery. We now show in single membrane patches generated from the somas of rat neurons that sodium influx through INaP is sufficient for activation of KNa channels, without substantial contribution from the transient sodium current or bulk [Na+]i. INaP was found to be active at cell membrane resting potentials, a finding that may explain why IKNa can be evoked from negative holding potentials. These results show an unanticipated role for INaP in activating a negative feedback system countering the excitable effects INaP; the interrelatedness of INaP and IKNa suggests new ways neurons can tune their excitability.