Traumatic injury alters opiate receptor binding in rat spinal cord

Abstract

Recent studies with dynorphin (an endogenous ligand for the κ-opiate receptor) and receptor-selective opiate antagonists have indicated a role for the κ-receptor in the pathophysiology of spinal cord injury. However, no studies have specifically examined opiate receptor binding in relation to spinal injury. In the present experiments, opiate receptor binding was measured in spinal cord after traumatic injury in rats using the selective radioligands [³H][D-Ala², D-Leu⁵]enkephalin (δ-receptor agonist); [³H][D-Ala², MePhe⁴, Gly-(ol)⁵]enkephalin (μ-receptor agonist); and [³H]ethylketocyclazocine (κ-receptor agonist). The specific binding of ethylketocyclazocine, but not the other agonists, showed a significant, time-dependent, and localized increase at the injury site. Since dynorphin, which has been implicated as an injury factor after spinal trauma, shows similar localized increases after spinal injury, the present data are consistent with the hypothesis that up-regulation of the κ-receptor after injury may contribute to the subsequent secondary injury process.