Calcium-Activated Potassium Channels at Nodes of Ranvier Secure Axonal Spike Propagation
Calcium-Activated Potassium Channels at Nodes of Ranvier Secure Axonal Spike Propagation
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DOI：
10.1016/j.celrep.2015.08.022
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发表时间：
2015-09-22
期刊：
影响因子：
8.8
通讯作者：
Clark, Beverley A.
中科院分区：
文献类型：
--
作者：
Gruendemann, Jan;Clark, Beverley A.
脑区之间的功能连接依赖于髓鞘轴突的远程信号。这是由跳跃式动作电位传播保证的，这基本上取决于朗维耶节点上钠通道的可用性。尽管在解剖学上，多种钾通道类型已经定位于大脑的髓鞘轴突，但它们在维持节点兴奋性方面的功能募集的直接证据很少。小脑浦肯野细胞为其在小脑核中的目标提供连续的输入，以大范围的速率可靠地传递轴突尖峰，这需要一个持续可用的节点钠通道池。我们表明，钙激活钾通道（IK， K(Ca)3.1）通过t型电压门控Ca2+电流在Ranvier节点的局部活动依赖性钙（Ca2+）内流募集，提供了一个强大的机制，可能反对节点的去极化阻滞，因此是确保自发放电的浦肯野细胞连续轴突生长的关键。
Functional connectivity between brain regions relies on long-range signaling by myelinated axons. This is secured by saltatory action potential propagation that depends fundamentally on sodium channel availability at nodes of Ranvier. Although various potassium channel types have been anatomically localized to myelinated axons in the brain, direct evidence for their functional recruitment in maintaining node excitability is scarce. Cerebellar Purkinje cells provide continuous input to their targets in the cerebellar nuclei, reliably transmitting axonal spikes over a wide range of rates, requiring a constantly available pool of nodal sodium channels. We show that the recruitment of calcium-activated potassium channels (IK, K(Ca)3.1) by local, activity-dependent calcium (Ca2+) influx at nodes of Ranvier via a T-type voltage-gated Ca2+ current provides a powerful mechanism that likely opposes depolarizing block at the nodes and is thus pivotal to securing continuous axonal spike propagation in spontaneously firing Purkinje cells.