APOPTOSIS AND EXPRESSION OF BCL-2 AFTER COMPRESSION TRAUMA TO RAT SPINAL-CORD

We have evaluated by in situ nick-end labeling the presence of apoptot ic cells in the spinal cord of rats with compression injury at the lev el of Th-8-9 of mild, moderate, and severe degrees resulting in no neu rologic deficit, reversible paraparesis, and paraplegia, respectively. Rats with compression injury surviving 4 or 9 days showed apoptotic g lial cells in the longitudinal tracts of the Th-8-9, the cranial Th-7, and the caudal Th-10 segments. The apoptotic cells were most frequent ly observed in Th-7. They did not express glial fibrillar acidic prote in (GFAP) and their morphology was compatible with that of oligodendro cytes. Neurons of the gray matter did not present signs of apoptosis. In addition, we studied the immunohistochemical expression of Bcl-2, a n endogenous inhibitor of apoptosis. Compression induced Bcl-2 immunor eactivity in axons of the long tracts, particularly after moderate and severe compression and I-day survival. Neurons of dorsal root ganglia were immunoreactive but the neurons of the spinal cord were unstained . The accumulation, presumably caused by arrested axonal transport in sensory pathways, was absent in rats surviving 9 days. In conclusion, compression trauma to rat spinal cord induces signs of apoptosis in gl ial cells, presumably oligodendrocytes of the long tracts. This may in duce delayed myelin degeneration after trauma to the spinal cord. Bcl- 2 does not seem to be upregulated in oligodendrocytes.