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树突棘(dendritic spine)是位于神经元树突分支上的微小功能性突起结构,参与神经元之间信息传递,也被视为中枢神经系统突触结构可塑性的基础。帕金森病(Parkinson’s disease,PD)动物模型纹状体中等多棘神经元(medium spiny neurons,MSNs)树突棘形态结构发生异常改变,且与运动功能障碍的出现具有一致性。运动调节基底神经节功能紊乱,有效改善PD行为功能障碍的神经生物学机制可能与纹状体MSNs树突棘形态结构重塑有关。本文拟从纹状体神经元构筑与树突棘形态结构特征、纹状体MSNs树突棘形态结构异常与PD、运动与PD纹状体MSNs树突棘形态结构重塑以及AMPARs介导PD纹状体MSNs树突棘运动依赖性重塑四个方面对纹状体MSNs树突棘形态结构可塑性在PD运动防治中的作用进行综述。
Dendritic spine is a tiny functional protuberance located on the dendritic branch of neurons involved in the transmission of information between neurons and is also considered as the basis of plasticity of the synaptic structure of the central nervous system. In the Parkinson’s disease (PD) animal model, the morphological changes of dendritic spines in the middle splenic neurons of the striatum were abnormally changed, and they were consistent with the appearance of motor dysfunction. The neurobehavioral mechanisms that regulate motor dysfunction of basal ganglia and effectively improve PD behavioral dysfunction may be related to remodeling of dendritic spine morphology of striatum. This article from the striatum neurons to construct and dendritic spine morphological features, striatum MSNs dendritic spine morphological abnormalities and PD, motor and PD striatum MSNs dendritic spine morphological remodeling and AMPARs mediated PD pattern In this study, we reviewed the role of morphological plasticity of dendritic spines in striatum in PD motility control in four aspects.