Wang Qiang, Zhang Wangming
The National Key Clinic Specialty, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Front Neural Circuits. 2016 Dec 20;10:105. doi: 10.3389/fncir.2016.00105. eCollection 2016.
The emergence of L-DOPA-induced dyskinesia (LID) in patients with Parkinson disease (PD) could be due to maladaptive plasticity of corticostriatal synapses in response to L-DOPA treatment. A series of recent studies has revealed that LID is associated with marked morphological plasticity of striatal dendritic spines, particularly cell type-specific structural plasticity of medium spiny neurons (MSNs) in the striatum. In addition, evidence demonstrating the occurrence of plastic adaptations, including aberrant morphological and functional features, in multiple components of cortico-basal ganglionic circuitry, such as primary motor cortex (M1) and basal ganglia (BG) output nuclei. These adaptations have been implicated in the pathophysiology of LID. Here, we briefly review recent studies that have addressed maladaptive plastic changes within the cortico-BG loop in dyskinetic animal models of PD and patients with PD.
帕金森病（PD）患者中左旋多巴诱导的异动症（LID）的出现可能是由于皮质纹状体突触对左旋多巴治疗产生的适应性不良可塑性。最近的一系列研究表明，LID与纹状体树突棘的显著形态可塑性有关，特别是纹状体中中等棘状神经元（MSN）的细胞类型特异性结构可塑性。此外，有证据表明，在皮质-基底神经节回路的多个组成部分，如初级运动皮层（M1）和基底神经节（BG）输出核中，发生了包括异常形态和功能特征在内的可塑性适应。这些适应与LID的病理生理学有关。在这里，我们简要回顾了最近的研究，这些研究探讨了PD异动症动物模型和PD患者皮质-基底神经节回路内的适应性不良可塑性变化。
