Delayed peripheral Nerve Degeneration, Regeneration, and pain in Mice Lacking Inducible Nitric Oxide Synthase (original) (raw)

Journal Article

Dan Levy, PHD ,

Department of Clinical Neurosciences and the Neuroscience Research Group,

University of Calgary

, Calgary, Alberta, Canada

Correspondence to: Dr. D.W. Zochodne, University of Calgary, Department of Clinical Neurosciences, Room 182A, 3330 Hospital Drive, NW, Calgary, Alberta T2N 4N1 Canada.

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Paul Kubes, PHD ,

Departments of physiology and Biophysics and the Immunology Research Group,

University of Calgary

, Calgary, Alberta, Canada

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Douglas W. Zochodne, MD, FRCPC

Douglas W. Zochodne, MD, FRCPC

Department of Clinical Neurosciences and the Neuroscience Research Group,

University of Calgary

, Calgary, Alberta, Canada

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Received:

26 September 2000

Revision received:

16 January 2001

Accepted:

24 January 2001

Cite

Dan Levy, Paul Kubes, Douglas W. Zochodne, Delayed peripheral Nerve Degeneration, Regeneration, and pain in Mice Lacking Inducible Nitric Oxide Synthase, Journal of Neuropathology & Experimental Neurology, Volume 60, Issue 5, May 2001, Pages 411–421, https://doi.org/10.1093/jnen/60.5.411
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Abstract

Inducible nitric oxide synthase (iNOS) may be a critical factor in the repair of injured tissues. In mice lacking iNOS we observed abnormalities in how the peripheral nerve responds to each of 3 fundamental types of injury: chronic constriction partial nerve injury (a model of neuropathic pain), nerve crush, and nerve transection. In each type of injury, mice lacking iNOS had evidence of a regenerative delay, preceded by slowing of myelinated fiber Wallerian degeneration (WD). In wild-type mice, iNOS immunoreactivity and the presence and upregulation of its mRNA were demonstrated distal to injury, but neither was observed in the knockout mice. Slowed WD was suggested by the abnormal persistence of apparent myelinated fiber profiles distal to the injury zones in mice lacking iNOS compared to wild-type controls. In mice lacking iNOS there were fewer regenerating myelinated fibers, smaller caliber regenerating fibers, and slowed reinnervation of muscle endplates distal to the injury zone. Slowed degeneration was also associated with normal initiation but delayed expression of neuropathic pain. Our findings highlight important relationships among nitric oxide, WD, neuropathic pain, and axon regeneration.

Copyright © 2001 by the American Association of Neuropathologists

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