Injury in the spinal cord may produce cell death in the brain.
Functional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute spinal cord injury (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 SCI model. Rats were laminectomized and SCI was induced using NYU spinal impactor at T9 segment. The behavioral test was performed. Electrophysiologically, motor evoked potentials (MEPs) were recorded. The animals were subjected to morphological study at 12, 24, 48, 72 h, and 1 week, postoperatively. Locomotor deficits were observed after SCI, and changes in the amplitudes and latencies of the MEPs were observed. The morphological changes were evidenced by terminal TUNEL staining and Calbindin-D(28K) immunohistochemistry. The TUNEL-positive cells were located at the brain motor cortex after SCI. TUNEL-positive cells were seldom found 4 h after injury. In addition, Calbindin-D28K immunoreactive neurons were observed in the motor cortex after injury. 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 that were deteriorated after SCI may be related to these electrophysiological and morphological changes.
Lee
Bae Hwan
BH
Department of Neurosurgery, Medical Research Center, Brain Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, C.P.O. Box 8044, Seoul 120-752, South Korea.
Lee
Kyung Hee
KH
Kim
Un Jeng
UJ
Yoon
Do Heum
DH
Sohn
Jin-Hun
JH
Choi
Sang Sup
SS
Yi
Im-Gap
IG
Park
Yong Gou
YG
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D064092:Calbindin 1; D064026:Calbindins; D019054:Evoked Potentials, Motor; D020287:In Situ Nick-End Labeling; D008297:Male; D009044:Motor Cortex / Q000473:pathology*; D009046:Motor Neurons / Q000473:pathology*; D009415:Nerve Net / Q000473:pathology; D009419:Nerve Tissue Proteins; D051381:Rats; D017207:Rats, Sprague-Dawley; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology*
C576500:Calb1 protein, rat; D064092:Calbindin 1; D064026:Calbindins; D009419:Nerve Tissue Proteins; D064030:S100 Calcium Binding Protein G