强啡肽对大鼠行为学和脊髓组织学改变的影响及受体机制

目的探明强啡肽(Dyn)对脊髓的损伤效应及其受体机制。方法观测大鼠鞘内注射DynA(1-13)或联合注射Kappa阿片受体拮抗剂nor-BNI或兴奋性氨基酸(EAA)的NMDA受体拮抗剂MK-801后的运动功能和脊髓病理学变化。结果注射30nmolDyn组3d时,Tarlov运动功能评分下降,脊髓前角神经元数目减少,GFAP阳性神经胶质细胞数轻度增生。14d时,Tarlov运动功能评分未恢复,神经胶质细胞增生明显。而鞘内联合注射100nmol nor-BNI、100nmol MK-801后3d时与单纯Dyn组结果相似,14d时Tarlov运动功能评分明显恢复,脊髓前角神经元数目较Dyn组多,GFAP阳性神经胶质细胞增生不明显,nor-BNI组与MK-801组间比较差异不显著。结论Dyn鞘内注射可使大鼠运动功能、脊髓组织损害,而nor-BNI或MK-801有对抗其损害作用。Dyn的病理作用是通过Kappa阿片受体和EAA的NMDA受体两种途径介导的。

Effects and receptor mechanism of dynorphin-induced changes of behavior and spinal cord histology of rat

ObjectiveTo explore the injury effects and receptor mechanism of dynorphin (Dyn) on spinal cord. MethodsQuantitative studies were performed to determine the changes of motor function and pathology of spinal cord induced by subarachnoid injection of DynA(1-13) or associated with NMDA receptor antagonist MK-801 or associated with Kappa receptor antagonist nor-BNI. ResultsSuch changes as decrease of Talov score and neurons in spinal cord anterior horn and increase of GFAP-positive neuroglial cells were found in the group of 30nmol DynA(1-13) injected. When associated with injection of 100nmol MK-801 or 100nmol nor-BNI, similar changes occurred at 3d and minor changes were found at 14d, which were significantly different from group DynA(1-13). There was no significantly statistical difference between group MK-801 and group nor-BNI. ConclusionIntrathecal injection of Dyn can induce lesion of motor function and spinal cord histology. MK-801 and nor-BNI can relieve the injury effect of DynA(1-13). Effects of Dyn are mediated by both Kappa and NMDA receptor.