Apoptosis and expression of Bcl-2 after compression trauma to rat spinal cord.

摘要: We have evaluated by in situ nick-end labeling the presence of apoptotic cells spinal cord rats with compression injury at level Th8-9 mild, moderate, and severe degrees resulting no neurologic deficit, reversible paraparesis, paraplegia, respectively. Rats surviving 4 or 9 days showed glial longitudinal tracts Th8-9, cranial Th7, caudal Th10 segments. The were most frequently observed Th7. They did not express fibrillar acidic protein (GFAP) their morphology was compatible that oligodendrocytes. Neurons gray matter present signs apoptosis. In addition, we studied immunohistochemical expression Bcl-2, an endogenous inhibitor Compression induced Bcl-2 immunoreactivity axons long tracts, particularly after moderate 1-day survival. dorsal root ganglia immunoreactive but neurons unstained. accumulation, presumably caused arrested axonal transport sensory pathways, absent days. conclusion, trauma to rat induces apoptosis cells, oligodendrocytes tracts. This may induce delayed myelin degeneration cord. does seem be upregulated