title: Chronic nerve compression alters Schwann cell myelin architecture in a murine model.
abstract: BACKGROUND
  Myelinating Schwann cells compartmentalize their outermost layer to form actin-rich channels known as Cajal bands. Herein we investigate changes in Schwann cell architecture and cytoplasmic morphology in a novel mouse model of carpal tunnel syndrome.
  
  
  METHODS
  Chronic nerve compression (CNC) injury was created in wild-type and slow-Wallerian degeneration (Wld(S) ) mice. Over 12 weeks, nerves were electrodiagnostically assessed, and Schwann cell morphology was thoroughly evaluated.
  
  
  RESULTS
  A decline in nerve conduction velocity and increase in g-ratio is observed without early axonal damage. Schwann cells display shortened internodal lengths and severely disrupted Cajal bands. Quite surprisingly, the latter is reconstituted without improvements to nerve conduction velocity.
  
  
  CONCLUSIONS
  Chronic entrapment injuries like carpal tunnel syndrome are primarily mediated by the Schwann cell response, where decreases in internodal length and myelin thickness disrupt the efficiency of impulse propagation. Restitution of Cajal bands is not sufficient for remyelination after CNC injury.
authors.affiliation: Department of Orthopaedic Surgery, University of California at Irvine, 2226 Gillespie Neuroscience Research Facility, Irvine, California 92697, USA. ranjang@uci.edu
authors.forename: Ranjan
authors.initials: R
authors.lastname: Gupta
authors.forename: Nima
authors.initials: N
authors.lastname: Nassiri
authors.forename: Antony
authors.initials: A
authors.lastname: Hazel
authors.forename: Mary
authors.initials: M
authors.lastname: Bathen
authors.forename: Tahseen
authors.initials: T
authors.lastname: Mozaffar
mesh_terms: D000199:Actins / Q000378:metabolism; D000200:Action Potentials; D000704:Analysis of Variance; D000818:Animals; D001369:Axons / Q000473:pathology; D002349:Carpal Tunnel Syndrome / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D003599:Cytoskeleton / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004576:Electromyography; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008818:Mice, Neurologic Mutants; D009186:Myelin Sheath / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009431:Neural Conduction / Q000502:physiology; D012583:Schwann Cells / Q000473:pathology*; D012584:Sciatic Nerve / Q000378:metabolism / Q000473:pathology; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D000199:Actins; D036341:Intercellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; C442580:Wld protein, mouse; C095114:collapsin response mediator protein-2