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慢性周围神经受压会破坏结旁轴突-神经胶质连接。

Chronic peripheral nerve compression disrupts paranodal axoglial junctions.

作者信息

Otani Yoshinori, Yermakov Leonid M, Dupree Jeffrey L, Susuki Keiichiro

机构信息

Department of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.

Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.

出版信息

Muscle Nerve. 2017 Apr;55(4):544-554. doi: 10.1002/mus.25273. Epub 2016 Dec 26.

Abstract

INTRODUCTION

Peripheral nerves are often exposed to mechanical stress leading to compression neuropathies. The pathophysiology underlying nerve dysfunction by chronic compression is largely unknown.

METHODS

We analyzed molecular organization and fine structures at and near nodes of Ranvier in a compression neuropathy model in which a silastic tube was placed around the mouse sciatic nerve.

RESULTS

Immunofluorescence study showed that clusters of cell adhesion complex forming paranodal axoglial junctions were dispersed and overlapped frequently with juxtaparanodal components. These paranodal changes occurred without internodal myelin damage. The distribution and pattern of paranodal disruption suggests that these changes are the direct result of mechanical stress. Electron microscopy confirmed loss of paranodal axoglial junctions.

CONCLUSIONS

Our data show that chronic nerve compression disrupts paranodal junctions and axonal domains required for proper peripheral nerve function. These results provide important clues toward better understanding of the pathophysiology underlying nerve dysfunction in compression neuropathies. Muscle Nerve 55: 544-554, 2017.

摘要

引言

周围神经经常受到机械应力作用,从而导致压迫性神经病变。慢性压迫导致神经功能障碍的病理生理学机制在很大程度上尚不清楚。

方法

我们在一个压迫性神经病变模型中分析了郎飞结及其附近的分子组织和精细结构,该模型是在小鼠坐骨神经周围放置一个硅橡胶管。

结果

免疫荧光研究显示,形成结旁轴突-神经胶质连接的细胞粘附复合体簇分散,且经常与结旁旁成分重叠。这些结旁变化发生时,节间髓鞘并无损伤。结旁破坏的分布和模式表明,这些变化是机械应力的直接结果。电子显微镜证实了结旁轴突-神经胶质连接的丧失。

结论

我们的数据表明,慢性神经压迫会破坏周围神经正常功能所需的结旁连接和轴突区域。这些结果为更好地理解压迫性神经病变中神经功能障碍的病理生理学提供了重要线索。《肌肉与神经》55: 544 - 554, 2017年。

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