Dynorphin A (1-17) causes motor dysfunction and decreases adenylyl cyclase-cAMP level of spinal cord in rat

Influence of Dynorphin A (1-17) (Dyn) on motor function and adenylate cyclase (AC)-cAMP level after intrathecal injection (ith) were investigated. Dyn 5, 10, 20 nmol caused dose-dependent flaccid paralysis of hindlimbs. Dyn 10, 20 nmol decreased spinal adenylate cyclase (AC) activity and cyclic AMP production 10 min after ith. They recovered to varying extent two hours later. Pretreatment with selective κ-opioid receptor antagonist nor-BNI 30 nmol 10 min before Dyn significantly blocked the effects of Dyn 20 nmol on hindlimb paralysis and inhibition of AC-cAMP level; L-type Ca²⁺ channel blocker verapamil 100 nmol also played a role in blocking Dyn neurotoxicity while NMDA receptor antagonist APV 10 nmol had no effect. The results showed that κ-opioid receptor and Ca²⁺ channel play a role in spinal cord injury and regulation of AC-cAMP level by Dyn.