Functional and structural properties of ion channels at the nerve terminal depends on compact myelin
Functional and structural properties of ion channels at the nerve terminal depends on compact myelin
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DOI：
10.1113/jp272205
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发表时间：
2016-10-01
影响因子：
5.5
通讯作者：
Kim, Jun Hee
中科院分区：
文献类型：
--
作者：
Berret, Emmanuelle;Kim, Sei Eun;Kim, Jun Hee
轴突髓鞘形成增加传导速度和动作电位传播的精确性。虽然脱髓鞘的负面影响通常归因于传导失败，但越来越多的证据表明髓鞘形成也调节轴突膜的结构特性和分子组成。在本研究中，我们研究了髓鞘形成如何影响离子通道的表达和功能，特别是在神经末梢前的最后一个轴突半节点，其调节神经末梢的突触前兴奋性。我们比较了正常轴突和缺乏致密髓鞘的Long-Evans Shaker（LES）大鼠的轴突的结构和生理。在LES大鼠中，半结和末端的Na+通道表达和动力学的正常分离丢失。具体而言，Na（V）4亚基是分散的，而Na（V）4亚基是缺乏的，而K+通道的密度增加，在半节点。相应地，复苏和持续的Na+电流减少，K+电流增加。两者合计，这些数据表明，在编排的离子通道的表达和功能在轴突半节点和调节神经末梢的兴奋性的致密髓鞘的特定作用。
Axon myelination increases the conduction velocity and precision of action potential propagation. Although the negative effects of demyelination are generally attributed to conduction failure, accumulating evidence suggests that myelination also regulates the structural properties and molecular composition of the axonal membrane. In the present study, we investigated how myelination affects ion channel expression and function, particularly at the last axon heminode before the nerve terminal, which regulates the presynaptic excitability of the nerve terminal. We compared the structure and physiology of normal axons and those of the Long-Evans shaker (LES) rat, which lacks compact myelin. The normal segregation of Na+ channel expression and dynamics at the heminode and terminal was lost in the LES rat. Specifically, Na-V- subunits were dispersed and Na(V)4 subunit was absent, whereas the density of K+ channels was increased at the heminode. Correspondingly, resurgent and persistent Na+ currents were reduced and K+ current was increased. Taken together, these data suggest a specific role for compact myelin in the orchestration of ion channel expression and function at the axon heminode and in regulating excitability of the nerve terminal.