The effect and mecbanism of kappa opiate receptor agonist and high-frequency electrostimulation of acupoints in treating spinal spasticity were studied. The spinal spastic models were made by gradual mechanical compression on the cervical spinal cord of rabbits. 24 prepared rabbits were divided into 3 groups randomly, and each group with 8 rabbits was given intrathecally kappa-receptor agonist 66A-078, kappa-receptor antagonist +66A-078 and normal saline respectively. The degree of spasticity was quantified by both clinical score and electrophysiological examinations. The result showed that the spasticity was markedly inhibited by intrathecal injection of 66A-078 and that the kappa-receptor antagonist (naloxone) reversed this effect. We can infer that the antispastic effect of 66A-078 is mediated by kappa-receptors. This result is helpful in explaining the immediate antispastic mechanism of high-frequency electrostimniation of acupaints discussed in previous study. The effect and mecbanism of kappa opiate receptor agonist and high-frequency electrostimulation of acupoints in treating spinal spasticity were studied. The spinal spastic models were made by gradual mechanical compression on the cervical spinal cord of rabbits. 24 prepared rabbits were divided into 3 groups randomly , and each group with 8 rabbits was given intrathecally kappa-receptor agonist 66A-078, kappa-receptor antagonist + 66A-078 and normal saline respectively. The degree of spasticity were quantified by both clinical score and electrophysiological examinations. The result showed that the spasticity was markedly inhibited by intrathecal injection of 66A-078 and that the kappa-receptor antagonist (naloxone) reversed effect. We can infer that the antispastic effect of 66A-078 is mediated by kappa-receptors. This result is helpful in explaining the immediate antispastic mechanism of high-frequency electrostimiation of acupaints discussed in previous study.