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髓鞘化外周轴突的兴奋性能持续增加是由 Nav1.6 介导的。

Sustained increase in the excitability of myelinated peripheral axons to depolarizing current is mediated by Nav1.6.

机构信息

Institute of Physiology, University of Munich, Pettenkoferstr. 12, D-80336 Munich, Germany.

出版信息

Neurosci Lett. 2011 Apr 4;492(3):129-33. doi: 10.1016/j.neulet.2011.01.069. Epub 2011 Feb 2.

DOI:10.1016/j.neulet.2011.01.069
PMID:21295113
Abstract

Changes in the excitability of peripheral myelinated axons in response to long-lasting subthreshold depolarizing or hyperpolarizing currents (threshold electrotonus) are used as a complementary electrophysiological parameter in the study of peripheral nerve diseases in people. However, the contribution made by various axonal ion channels to specific components of threshold electrotonus remains incompletely understood. In this study, we have recorded threshold electrotonus responses from isolated nerve segments of sural nerve from control and Scn8amed mice, which lack functional Nav1.6 voltage-gated sodium channel. In med mice, the increase in axonal excitability produced by application of subthreshold depolarizing currents for 100-200ms was not sustained. In contrast, there was no difference in threshold electrotonus responses to subthreshold hyperpolarizing current application between Scn8amed and control mice. These data reveal the specific functional role of an identified subtype of voltage-gated sodium channel (Nav1.6) in mediating the depolarizing threshold electrotonus response of peripheral myelinated nerve fibers.

摘要

外周有髓神经纤维的兴奋性在长时阈下去极化或超极化电流(阈电紧张)作用下的变化,被用作研究人类周围神经疾病的一种补充电生理参数。然而,各种轴突离子通道对阈电紧张特定成分的贡献仍不完全清楚。在这项研究中,我们记录了来自对照和 Scn8amed 小鼠(缺乏功能性 Nav1.6 电压门控钠离子通道)的腓肠神经分离神经节段的阈电紧张反应。在 med 小鼠中,应用阈下去极化电流 100-200ms 产生的轴突兴奋性增加不能维持。相比之下,Scn8amed 和对照小鼠对阈下超极化电流应用的阈电紧张反应没有差异。这些数据揭示了特定类型的电压门控钠离子通道(Nav1.6)在介导周围有髓神经纤维去极化阈电紧张反应中的特定功能作用。

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