THE OLIGODENDROGLIAL REACTION TO BRAIN STAB WOUNDS - AN IMMUNOHISTOCHEMICAL STUDY

Citation
Dc. Xie et al., THE OLIGODENDROGLIAL REACTION TO BRAIN STAB WOUNDS - AN IMMUNOHISTOCHEMICAL STUDY, Journal of neurocytology, 24(6), 1995, pp. 435-448
Citations number
22
Categorie Soggetti
Neurosciences,"Cell Biology
Journal title
ISSN journal
03004864
Volume
24
Issue
6
Year of publication
1995
Pages
435 - 448
Database
ISI
SICI code
0300-4864(1995)24:6<435:TORTBS>2.0.ZU;2-P
Abstract
Myelin/oligodendrocyte specific protein was compared to glial fibrilla ry acidic protein and 2'3'-cyclic nucleotide 3'-phosphodiesterase expr ession in normal rat brains and following stab wounds to the cerebral cortex, corpus callosum and hippocampus. Animals with stab wounds were allowed to recover for 5, 15, 28, 45 and 70 days post-operation befor e fixation by perfusion. Sections were reacted with antibodies against myelin/oligodendrocyte specific protein, glial fibrillary acidic prot ein and 2'3'-cyclic nucleotide 3'-phosphodiesterase, and observed by l ight and electron microscopy. Normal cerebral cortex had very few myel in/oligodendrocyte specific protein-positive and 2'3'-cyclic nucleotid e 3'-phosphodiesterase-positive cells, but some glial fibrillary acidi c protein-positive cells. The myelinated fibres of the corpus callosum were heavily stained for myelin/oligodendrocyte specific protein but unstained by glial fibrillary acidic protein or 2'3'-cyclic nucleotide 3'-phosphodiesterase antibodies. Some immunopositive cells were prese nt in the corpus callosum and hippocampus with all three antibodies. A fter stab wound myelin/oligodendrocyte specific protein-positive react ive cells had more and longer processes and stained more intensely tha n equivalent cells in normal brain. These cells were distributed along the wound track, including within the cerebral cortex. The numbers of these cells increased until 28 days post-operation and then decreased so that very few were found at 70 days post-operation except in the c orpus callosum. Where demyelination occurred myelin/oligodendrocyte sp ecific protein-staining was lost. Staining for 2' 3'-cyclic nucleotide 3'-phosphodiesterase revealed a similar pattern. Glial fibrillary aci dic protein-positive reactive cells, which were also more robust than the normal cells, were more widely distributed. They increased in numb er throughout the time periods studied and gliosis was evident on the contralateral side. The glial fibrillary acidic protein-positive astro cytes were also different from the myelin/oligodendrocyte specific pro tein-positive and 2'3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendrocytes in terms of cell shape. With electron microscopy mye lin/oligodendrocyte specific protein-positive cells showed features ty pical of immature oligodendrocytes. We conclude that the injury caused a numerical increase in oligodendrocytes and that myelin/oligodendroc yte specific protein is a good marker for the oligodendroglial respons e and demyelination in pathological conditions.