The oligodendroglial reaction to brain stab wounds: An immunohistochemical study

Abstract

Myelin/oligodendrocyte specific protein was compared to glial fibrillary acidic protein and 2'3'-cyclic nucleotide 3'-phosphodiesterase expression 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 before fixation by perfusion. Sections were reacted with antibodies against myelin/oligodendrocyte specific protein, glial fibrillary acidic protein and 2'3'-cyclic nucleotide 3'-phosphodiesterase, and observed by light and electron microscopy. Normal cerebral cortex had very few myelin/oligodendrocyte specific protein-positive and 2'3'-cyclic nucleotide 3'-phosphodiesterase-positive cells, but some glial fibrillary acidic 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 present in the corpus callosum and hippocampus with all three antibodies. After stab wound myelin/oligodendrocyte specific protein-positive reactive cells had more and longer processes and stained more intensely than 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 corpus callosum. Where demyelination occurred myelin/oligodendrocyte specific protein-staining was lost. Staining for 2'3-cyclic nucleotide 3'-phosphodiesterase revealed a similar pattern. Glial fibrillary acidic protein-positive reactive cells, which were also more robust than the normal cells, were more widely distributed. They increased in number throughout the time periods studied and gliosis was evident on the contralateral side. The glial fibrillary acidic protein-positive astrocytes were also different from the myelin/oligodendrocyte specific protein-positive and 2'3'-cyclic nucleotide 3'-phosphodiesterase-positive oligodendrocytes in terms of cell shape. With electron microscopy myelin/oligodendrocyte specific protein-positive cells showed features typical of immature oligodendrocytes. We conclude that the injury caused a numerical increase in oligodendrocytes and that myelin/oligodendrocyte specific protein is a good marker for the oligodendroglial response and demyelination in pathological conditions.

Oligodendroglial reaction following spinal cord injury in rat: Transient upregulation of MBP mRNA

“…The post-injury reaction of oligodendrocytes is poorly understood. Proliferation of oligodendrocytes has been shown following stab wound lesion in the brain, indicating that they might undergo an attempt for repair (Ludwin, 1984(Ludwin, , 1985Xie et al, 1995). However, it is not known whether this proliferative response takes place also in other CNS compartments (e.g., the spinal cord) or whether it actually leads to increased myelin synthesis.…”

Ischemic Damage and Subsequent Proliferation of Oligodendrocytes in Hippocampal CA1 Region following Repeated Brief Cerebral Ischemia

“…Although oligodendrocytes can respond to damage and proliferate in the brain following trauma [7,23] , and transplantation of 0-2A progenitor cells [28] or cultured oligodendrocytes [29] can repair demyelinating damage in the brain, the role of oligodendrocytes in the repair process after brain injury such as trauma and ischemia has not been fully investigated. Mandai et al [8] demonstrated accumulation of oligodendrocytes in the ischemia-induced brain lesion with in situ hybridization histochemistry.…”

“…Ludwin and Sternberger [22] found that oligodendrocytes incorporated tritiated thymidine following cuprizone-induced demyelination. Xie et al [7] , after brain stab wounds, found that the number of reactive oligodendrocytes along the wound track increased until 28 days after operation, and then decreased so that very few were found at 70 days after operation. In contrast, the number of GFAP-positive cells continued to increase throughout the time period's studies.…”

“…Full recovery of function following injury to the CNS requires oligodendroglial regeneration. Under some conditions, oligodendroglial proliferation is possible in adult brain such as virus-induced damage [21] , cuprizone-derived lesions [22] , physical trauma [7,23] , multiple sclerosis [5,6] and focal cerebral ischemia [8] . Proliferation and hypertrophy of oligodendrocytes in the adult CNS under pathological conditions are presently of interest to neurobiolosists.…”

“…Although oligodendrocytes can respond to damage and proliferate in the brain, the role of oligodendrocytes in the repair process after brain injury such as trauma and ischemia has not been fully investigated. Xie et al [7] , after brain stab wounds, found that the number of reactive oligodendrocytes along the wound track increased until 28 days after operation. Mandai et al [8] described subsequent proliferation of oligodendrocytes in focal cerebral ischemia.…”