Na+-activated K+ channels express a large delayed outward current in neurons during normal physiology.
Na+-activated K+ channels express a large delayed outward current in neurons during normal physiology.
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DOI：
10.1038/nn.2313
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发表时间：
2009-06
影响因子：
25
通讯作者：
Salkoff, Lawrence
中科院分区：
文献类型：
--
作者：
Budelli, Gonzalo;Hage, Travis A.;Wei, Aguan;Rojas, Patricio;Jong, Yuh-Jiin Ivy;O'Malley, Karen;Salkoff, Lawrence
在许多哺乳动物神经元中，延迟外向电流的最大成分之一在正常生理过程中被激活，如纹状体的中等刺神经元和嗅球的簇状二尖瓣细胞，但没有被注意到，这是由于Na+激活的K+电流。以前对哺乳动物神经元K+电流的研究可能忽略了这一大的外向成分，因为钠通道阻滞剂河豚毒素(TTX)通常用于此类研究；我们发现TTX也消除了这种延迟的外向成分作为次要结果。出乎意料的是，我们发现持续的内向钠电流(Persistent Intra)的活性在激活这种大的钠离子依赖(TTX敏感)的延迟外向电流时非常有效。利用siRNA技术，我们确定SLO2.2(Slack)通道是这种延迟外向电流的载体。这些发现对细胞和系统神经科学的许多方面，以及临床神经学和药理学都有深远的影响。
One of the largest components of the delayed outward current active during normal physiology in many mammalian neurons such as medium spiny neurons of the striatum and tufted–mitral cells of the olfactory bulb, has gone unnoticed and is due to a Na+-activated-K+-current. Previous studies of K+ currents in mammalian neurons may have overlooked this large outward component because the sodium channel blocker tetrodotoxin (TTX) is typically used in such studies; we find that TTX also eliminates this delayed outward component as a secondary consequence. Unexpectedly we found that the activity of a persistent inward sodium current (persistent INa) is highly effective in activating this large Na+-dependent (TTX-sensitive) delayed outward current. Using siRNA techniques we identified SLO2.2 (Slack) channels as carriers of this delayed outward current. These findings have far reaching implications for many aspects of cellular and systems neuroscience, as well as clinical neurology and pharmacology.
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