title: Pathological changes in the white matter after spinal contusion injury in the rat.
abstract: It has been shown previously that after spinal cord injury, the loss of grey matter is relatively faster than loss of white matter suggesting interventions to save white matter tracts offer better therapeutic possibilities. Loss of white matter in and around the injury site is believed to be the main underlying cause for the subsequent loss of neurological functions. In this study we used a series of techniques, including estimations of the number of axons with pathology, immunohistochemistry and mapping of distribution of pathological axons, to better understand the temporal and spatial pathological events in white matter following contusion injury to the rat spinal cord. There was an initial rapid loss of axons with no detectable further loss beyond 1 week after injury. Immunoreactivity for CNPase indicated that changes to oligodendrocytes are rapid, extending to several millimetres away from injury site and preceding much of the axonal loss, giving early prediction of the final volume of white matter that survived. It seems that in juvenile rats the myelination of axons in white matter tracts continues for some time, which has an important bearing on interpretation of our, and previous, studies. The amount of myelin debris and axon pathology progressively decreased with time but could still be observed at 10 weeks after injury, especially at more distant rostral and caudal levels from the injury site. This study provides new methods to assess injuries to spinal cord and indicates that early interventions are needed for the successful sparing of white matter tracts following injury.
authors.affiliation: Department of Pharmacology, University of Melbourne, Parkville, Victoria, Australia. cjek@unimelb.edu.au
authors.forename: C Joakim
authors.initials: CJ
authors.lastname: Ek
authors.forename: Mark D
authors.initials: MD
authors.lastname: Habgood
authors.forename: Ross
authors.initials: R
authors.lastname: Dennis
authors.forename: Katarzyna M
authors.initials: KM
authors.lastname: Dziegielewska
authors.forename: Carina
authors.initials: C
authors.lastname: Mallard
authors.forename: Benjamin
authors.initials: B
authors.lastname: Wheaton
authors.forename: Norman R
authors.initials: NR
authors.lastname: Saunders
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000473:pathology*; D003288:Contusions / Q000473:pathology; D007150:Immunohistochemistry / Q000379:methods; D007211:Indoles / Q000494:pharmacology; D008954:Models, Biological; D008959:Models, Neurological; D009186:Myelin Sheath / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D009836:Oligodendroglia / Q000166:cytology; D051381:Rats; D013116:Spinal Cord / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000473:pathology*
chemical_list: D007211:Indoles; C018588:Luxol Fast Blue MBS