Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-5-29
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
411-21
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Delayed peripheral nerve degeneration, regeneration, and pain in mice lacking inducible nitric oxide synthase.
pubmed:affiliation
Department of Clinical Neurosciences and the Neuroscience Research Group, University of Calgary, Alberta, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't