Volume 55, Issue 4 pp. 544-554
Basic & Translational Science

Chronic peripheral nerve compression disrupts paranodal axoglial junctions

Yoshinori Otani PhD

Yoshinori Otani PhD

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

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Leonid M. Yermakov BS

Leonid M. Yermakov BS

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

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Jeffrey L. Dupree PhD

Jeffrey L. Dupree PhD

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

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Keiichiro Susuki MD, PhD

Corresponding Author

Keiichiro Susuki MD, PhD

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

Correspondence to: K. Susuki; e-mail: [email protected]Search for more papers by this author
First published: 27 July 2016
Citations: 12

Funding: This work was supported by Veterans Affairs Merit Grant (5IO1BX002565 to J.L.D.) and National Institutes of Health (NIH) -National Institute of Neurological Disorders and Stroke Center Core Grant 5P30 NS047463.

Conflicts of Interest: The authors declare no competing financial interests.

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

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