Endogenous opioid immunoreactivity in rat spinal cord following traumatic injury

Abstract

It has been postulated that endogenous opioids play a pathophusiological role in spinal cord injury, based on the therapeutic effects of the opiate receptor antagonist naloxone in certain experimental models. The high doses of naloxone required to exert a therapeutic action suggest that naloxone's effects may be mediated by non-μ opiate receptors, such as the κ receptor. This notion is supported by recent than naloxone in improving outcome after spinal cord injury. Moreover, dynorphin-postulated to be the endogenous ligand for the κ receptor–is unique among opioids in producing hindlimn paralysis following intrathecal administration in the rat. In the present studies we have examined changes in endogenous opioid immunoreactivity following traumatic spinal cord injury in the rat. Dynorphin A was found to increase progressively with graded injury; changes were restricted to the injury segment and adjacent areas and were time dependent. Dynorphin A-(1–8) showed no marked changes. Mehtionine and leucine enkephalin were either unaltered or reduced at the injury site; changes were not well localized and were not clearly related to the injury variables. These findings provide further support for a potential pathophysiological role of prodynorphin-derived peptides in spinal cord injury.