ROLE OF CALPAIN IN SPINAL-CORD INJURY - INCREASED CALPAIN IMMUNOREACTIVITY IN SPINAL-CORD AFTER COMPRESSION INJURY IN THE RAT

Spinal cord injury was induced in rats by compression technique using 10 or 20 g compression for 5-10 min. Calpain immunoreactivity was examined in the lesion as well as in the adjacent areas of the cord at different times following injury. Elevated calpain immunoreactivity was found in the lesion compared to sham control. The increase in calpain immunoreactivity was dependent on the time and the degree of trauma. Areas adjacent posterior or caudal to the lesion also showed increased calpain immunoreactivity. Most of the cells in the dorsal and ventral funiculi with increased calpain staining were astrocytes and microglia. Proliferation of microglia and/or activation of astrocytes in the lesion, identified with lectin binding GSA and glial fibrillary acidic protein staining, was seen at 1 and 3 days after trauma, respectively. Eccentric nuclei and shrunken neurons with increased calpain staining were seen in the ventral horn. The extent of increase in calpain immunoreactivity in the lesion was also proportional to the degree of trauma. The elevated calpain immunoreactivity suggests increased calpain expression (mRNA), synthesis (protein level), and activity in the lesion of cord following injury as compared to sham control. This finding supports a pivotal role for calpain in tissue degeneration in spinal cord trauma.