The effect of intrathecal injection of dynorphin A （1-17） on second messenger systems of spinal cord relative to behavioral change in rats was studied. Dynorphin A （1-17） 5

10 （20nmol） caused dose-dependent flaccid paralysis of hindlimbs. Dynorphin A （1-17） 10

20 nmol dose-dependently decreased spinal adenylate cyclase （AC） activity

cyclic AMP production

calmodulin （CaM） level and cyclic-nucleotide phosphodiesterase（PDE）activity 10 min after intrathecal injection. They recovered to a varying extent two hours later. Pretreatment with selective κ-opioid receptor antagonist nor-BNI 30 nmol 10 min before dynorphin A （1-17） markedly antagonized the effects of dynorphin A （1-17 ） at 20 nmol on hindlimb paralysis and inhibition of intracellular second messengers. The L-type calcium channel blocker verapamil （100nmol） also played a role in blocking dynorphin neurotoxicity. The NMDA receptor antagonist APV could partially or completely block dynorphin inhibition of CaM level and PDE activity without affecting paralysis and decrease of AC-cAMP level induced by dynorphin A（1-17） 10 min after intrathecal injection.