Delayed peripheral nerve degeneration, regeneration, and pain in mice lacking inducible nitric oxide synthase

96Citations
Citations of this article
34Readers
Mendeley users who have this article in their library.

This article is free to access.

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.

Cite

CITATION STYLE

APA

Levy, D., Kubes, P., & Zochodne, D. W. (2001). Delayed peripheral nerve degeneration, regeneration, and pain in mice lacking inducible nitric oxide synthase. Journal of Neuropathology and Experimental Neurology, 60(5), 411–421. https://doi.org/10.1093/jnen/60.5.411

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free