Bcl-x(L) expression after contusion to the rat spinal cord

After contusion-derived spinal cord injury, (SCI) there is localized tissue disruption and energy failure that results in early necrosis and delayed a poptosis, events that contribute to chronic central pain in a majority of p atients. We assessed the extent of contusion-induced apoptosis of neurons i n a known central pain-signaling pathway, the spinothalamic tract (STT), wh ich may be a contributor to SCI-induced pain. We observed the loss of STT c ells and localized increase of DNA fragmentation and cytoplasmic histone-DN A complexes, which suggested potential apoptotic changes among STT neurons after SCI. We also showed SCI-associated changes in the expression of the a nti-apoptotic protein Bel-x(L), especially among STT cells, consistent with the hypothesis that Bcl-x(L) regulates the extent of apoptosis after SCI. Apoptosis in the injured spinal cord correlated well with prompt decreases in Bcl-x(L) protein levels and Bcl-x(L)/Bax protein ratios at the contusion site. We interpret these results as evidence that regulation of Bcl-x(L) m ay play a role in neural sparing after spinal injury and pain-signaling fun ction.