ERK1/2在左旋多巴诱导的异动症发生机制中的作用  

The Role of ERK1/2 in the pathogenesis of levodopa induced dyskinesia

作　　者：徐岩[1] 曹学兵[1] 黄若兰[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院神经内科,武汉430022

出　　处：《卒中与神经疾病》2008年第3期156-159,163,共5页Stroke and Nervous Diseases

基　　金：国家自然科学基金项目(No30300114)

摘　　要：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 study the role of extracellular regulated kinase 1/2（ERK1/2） and phosphorylated-ERK1/2（p-ERK1/2） in the molecular pathogenesis of LID（L-EK）PA induced dyskinesia）. Methods All rats were divided into five groups： normal control group, PD group, LID group, LID ＋ SCH23390 group and non-LID group. The behavioral changes were observed. The expression of ERK1/2 and p-ERK1/2 in striatum were measured and compared in each groups using immuno-histochemistry. Results Dopamine D1 receptor antagonist SCH23390 attenuated abnormal behavior of LID rats. ERK1/2 expression in LID rats was equal to non-LID group. LID rats expressed more p-ERKI/2 than PD rats and non-LID rats,which could be reduced by SCH23390. Conclusions ERK1/2 was an important signal cascade molecules in direct output pathway of striaturn in IAD rat, and its activity may be involved in pathogenesis of LID.

关 键 词：左旋多巴 异动症 ERK1/2多 巴胺D1受体 

分 类 号：R742.5[医药卫生—神经病学与精神病学] Q55[医药卫生—临床医学]