Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-7-17
pubmed:abstractText
The aim of this study was to elucidate whether oligodendrocytes die in fiber tracts that are spared by a spinal cord injury but are in close vicinity of inflammatory cells. Adult rat spinal cords were studied histologically 1 day to 2 weeks after a contusion lesion that left the ventral white matter largely intact. Massive oligodendrocyte death occurred in the lesion center, along with the death of neurons, microglia, and astrocytes. Oligodendrocytes, specifically positive for proteolipid protein (PLP) mRNA, were counted in the ventral white matter where axons at the rostral and caudal edges of the lesion were histologically intact. Although these regions contained many macrophages and neutrophils hypothesized to contribute to secondary tissue loss, there was no significant loss of oligodendrocytes. In the ventral funiculus, 3 and 6 mm rostral and caudal to the lesion, oligodendrocyte numbers were also unchanged, in spite of the presence of many activated microglial cells. From day 7 on, oligodendrocytes in close vicinity to the lesion increased their expression of PLP mRNA. We conclude that, at least within the first 2 weeks after a spinal cord contusion lesion, there is no major devastating influence of inflammatory cells or their mediators on oligodendrocytes. When death occurs, it may be due to mechanical trauma, ischemia, or excitotoxicity within the lesion or it may occur as a result of axonal degeneration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
373-80
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Reactions of oligodendrocytes to spinal cord injury: cell survival and myelin repair.
pubmed:affiliation
Brain Research Institute, Department Neuromorphology, Swiss Federal Institute of Technology, University of Zurich, Winterthurerstrasse 190, Zürich, 8057, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't