title: Chronic peripheral nerve compression disrupts paranodal axoglial junctions.
abstract: Peripheral nerves are often exposed to mechanical stress leading to compression neuropathies. The pathophysiology underlying nerve dysfunction by chronic compression is largely unknown.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Department of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Otani
authors.affiliation: Department of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
authors.forename: Leonid M
authors.initials: LM
authors.lastname: Yermakov
authors.affiliation: Department of Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, Virginia, USA.
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Dupree
authors.affiliation: Department of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Highway, Dayton, Ohio, 45435, USA.
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Susuki
mesh_terms: D000818:Animals; D017487:Ankyrins / Q000378:metabolism; D001176:Arthrogryposis / Q000473:pathology* / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D015816:Cell Adhesion Molecules, Neuronal / Q000378:metabolism; D004195:Disease Models, Animal; D019054:Evoked Potentials, Motor / Q000502:physiology*; D005260:Female; D007839:Functional Laterality; D005786:Gene Expression Regulation; D015417:Hereditary Sensory and Motor Neuropathy / Q000473:pathology* / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D046529:Microscopy, Electron, Transmission; D009414:Nerve Growth Factors / Q000378:metabolism; D009431:Neural Conduction / Q000502:physiology; D011901:Ranvier's Nodes / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D012584:Sciatic Nerve / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D051669:Shab Potassium Channels / Q000378:metabolism
chemical_list: C094681:Ank3 protein, mouse; D017487:Ankyrins; D015815:Cell Adhesion Molecules; D015816:Cell Adhesion Molecules, Neuronal; C491322:Cntnap1 protein, mouse; D009414:Nerve Growth Factors; C504593:Nfasc protein, mouse; D051669:Shab Potassium Channels; C520020:gliomedin protein, mouse
keywords: axon-glia interactions; compression neuropathy; mouse model; node of Ranvier; paranodal junction