There have been many efforts to maximize the recovery from spinal cord injury (SCI). The primary or mechanical insults seldom cause total transection, even though the functional loss may be complete in acute SCI. One of the main difficulties in the treatment of spinal cord injury has been that functional deficit has originated not only from direct physical damage, but also from secondary biochemical and pathological changes in the spinal cord. Cell death could be categorized as either necrosis or apoptosis. Over the past few years, evidence suggesting that the progression of ischemia in the brain may in part reflect apoptotic cell death has been reported. Apoptosis is frequently seen around the periphery of a spinal cord injury site and has been known to ultimately progress to necrosis and infarction as time lapses. We initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute SCI, and conducted a series of experiments the study examining the morphological changes in the brain following the spinal injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to spinal cord injury (SCI) model. Rats were laminectomized and spinal cord injury was induced using NYU spinal impactor at T9 segment. The behavioral tests such as BBB and inclined plain tests were performed. The animals were sacrifice periodically at 12, 24, 48, 72 hrs, 1 and 2 weeks, postoperatively. The morphorogical changes were evidenced by using cresylviolet staining, Tunel staining, immunohistochemistry (KD-28K, Bcl-2) and DNA fragmentaion. The TUNEL-positive cells were located at the brain motor cortex. No TUNEL-positive cells were found 4 hours after injury. Electrophoretic analysis of DNA extracts from the barin showed a laddering pattern, most prominent at 48 hours after SCI. These results suggest that apoptosis may play an important role in the pathophysiology of the brain motor cortex following acute spinal cord injury and functions deteriorated after SCI may spontaneously recover as time lapses. (Supported by KRF-99-042-F00109)
Source: Korean J Physiol Pharmacol.2001 Dec;5(Suppl II):S94
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