Bcl-xLExpression after Contusion to the Rat Spinal Cord

Abstract

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_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 may play a role in neural sparing after spinal injury and pain-signaling function.