Attenuation of Ciliary Neurotrophic Factor (CNTF) in Acute Spinal Cord Injury (ASCI) Treated with Intravenous Methylprednisolone (MP)

The effect(s) of steroid administration on second-pathway mediators associated with inflammation and repair following spinal cord injury have not been well characterized. We hypothesized that MP administration in a standard model of ASCI would inhibit CNTF expression at the site of injury. Sprague Dawley rats (n=24) were randomly divided into MP treated and control groups. Paraplegia after lower thoracic laminectomy was achieved using a standardized weight drop technique. Spinal cords were harvested at variable timed intervals from both groups and prepared for histologic/immunohistochemical evaluation after 23 hours of infusion. At both 0 and 8 hours post injury both groups demonstrated negative CNTF staining. At Twenty-Four and Forty-Eight hours respectively a consistent staining trend was appreciated. In the present experiment, MP treatment in a model of ASCI led to histologically evident inhibition of CNTF in spinal cord tissue by immunohistochemistry, 24-48 hours post-injury. The known role of CNTF as a neuronal repair and regenerative cytokine supports future studies to evaluate MP dosing regimens that inhibit spinal cord edema while optimizing CNTF expression.