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目的研究细胞外调节激酶(ERK1/2)在左旋多巴诱导的异动症(LID)发生机制中的作用。方法将SD大鼠分为5组:正常对照组、帕金森病(PD)组、LID组、LID+SCH23390组和非LID组,分别观察各组行为学变化,并用免疫组化方法测定大鼠纹状体区ERK1/2及其活化形式p-ERK1/2表达水平。结果多巴胺D1受体阻断剂SCH23390可以减轻LID大鼠行为学异常;LID组和非LID组ERK1/2的表达无显著性差异,而LID组p-ERK1/2的表达较非LID组和PD组明显增加,SCH23390使其表达下降。结论ERKI/2是LID大鼠纹状体内直接输出通路上的重要信号分子,其活化参与了异动症的发生。
Objective To investigate the role of extracellular regulated kinase (ERK1 / 2) in the mechanism of levodopa-induced dyskinesia (LID). Methods The SD rats were divided into 5 groups: normal control group, Parkinson’s disease (PD) group, LID group, LID + SCH23390 group and non-LID group. The changes of behavior were observed in each group, ERK1 / 2 in striatum and its activated form of p-ERK1 / 2 expression. Results SCH23390, a dopamine D1 receptor antagonist, could alleviate the behavioral abnormalities in LID rats. There was no significant difference in ERK1 / 2 expression between LID group and non-LID group, but the expression of p-ERK1 / 2 in LID group was significantly lower than that in non-LID group and PD Group was significantly increased, SCH23390 decreased its expression. Conclusion ERKI / 2 is an important signaling molecule in the direct output pathway of striatum of LID rats, whose activation is involved in the development of dyskinesia.