Bcl-x_Lexpression 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 apoptosis, events that contribute to chronic central pain in a majority of patients. We assessed the extent of contusion-induced apoptosis of neurons in a known central pain-signaling pathway, the spinothalamic tract (STT), which may be a contributor to SCI-induced pain. We observed the loss of STT cells and localized increase of DNA fragmentation and cytoplasmic histone-DNA complexes, which suggested potential apoptotic changes among STT neurons after SCI. We also showed SCI-associated changes in the expression of the antiapoptotic protein Bcl-x_Lespecially among STT cells, consistent with the hypothesis that Bcl-x_Lregulates the extent of apoptosis after SCI. Apoptosis in the injured spinal cord correlated well with prompt decreases in Bcl-x_Lprotein levels and Bcl-x_L/Bax protein ratios at the contusion site. We interpret these results as evidence that regulation of Bcl-x_Lmay play a role in neural sparing after spinal injury and pain-signaling function.