强啡肽对大鼠脊髓损伤的作用及其受体机制

目的 探明强啡肽（Dyn）在继发性脊髓损伤中的作用及其受体机制。方法观察鞘内注射DynA（1-13）或联合注射Kappa阿片受体拮抗剂卡匹帕明（nor-BNI）或兴奋性氨基酸（EAA）的NMDA受体拮抗剂MK-801后运动功能和脊髓前角神经元酶组织化学的变化。结果注射30nmol DynA（1-13）3d时，Rivlin斜板临界角变化增大，前角神经元酸性磷酸酶（ACP）活性增强；14d时，Rivlin斜板临界角变化未恢复，ACP活性轻度增强。鞘内联合注射100n mol nor-BNI、100n mol MK-801后3d，Rivlin斜板临界角增大和ACP活性增强，但在14d时Rivlin斜板临界角变化明显恢复、ACP活性接近正常，与Dyn组的差异有显著性；nor-BNI组与MK-801组的差异无显著性。结论Dyn鞘内注射可损害大鼠运动功能和脊髓组织，而nor-BNI或MK-801能对抗其损害作用。Dyn的病理作用是通过Kappa阿片受体和NMDA受体两种途径介导的。

Effects and receptor mechanism of dynorphin-induced injury of spinal cord

Objective To detect the injurious effects and receptor mechanism of dynorphin on secondary spinal cord injuries. Methods Quantitative studies were performed to determine the changes of motor function and enzymo-histochemistry of spinal cord neuron induced by subarachnoid injection of DynA(1-13) or associated NMDA receptor antagonist MK-801 or associated Kappa receptor antagonist nor-BNI. Results Such changes as increase of Rivlin tiltboard angle and reinforcement of spinal cord anterior horn neuron ACP activity were found in group 30 nmol DynA(1-13). The combined injection of 100 nmol MK-801 or 100 nmol nor-BNI, such changes also occurred at 3 d in mild degree, and minor changes were found at 2 w, which were significantly different from those of group DynA(1-13). There were no significant statistical difference between groups MK-801 and nor-BNI. Conclusions Intrathecal injection of dynorphin can induce motor function lesion and spinal cord tissue damage as shown by enzymo-histochemistry. MK-801 and nor-BNI can relieve the injurious effect of DynA(1-13). The effects of dynorphin are mediated through both Kappa and NMDA receptors.