Increased calpain content and progressive degradation of neurofilament protein in spinal cord injury.

Spinal cord injury was induced in rat by weight drop. The extent of degradation of neurofilament proteins in the lesion following trauma was examined and served as a measure of calpain activity. Calpain was identified in the samples by myelin mcalpain antibody and the content was estimated from the immunoblot. There was progressive degradation of both 68 kDa and 200 kDa neurofilament proteins in the cord lesion at intervals after injury. At 30 min after injury there was 20% degradation of both neurofilament proteins while the breakdown of 68 kDa and 200 kDa NFPs amounted to more than 60% at 24 h and beyond. Calpain content progressively increased in the lesion by 22% at 30 min to 91% at 4 h after trauma compared to control and then decreased but remained elevated for up to 72 h following injury. These results suggest that calpain is a primary responder synthesized early in injury and involved initially in the breakdown of cytoskeletal proteins in spinal cord trauma. Later in the injury cascade, increased calpain activity is derived from inflammatory as well as endogenous cells supporting a pivotal role for calpain throughout the process of secondary and evolving tissue damage in spinal cord trauma.