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作 者:牛轶瑄[1] 魏桂荣[1] 曹学兵[1] 袁光雷[1] 徐岩[1] 孙圣刚[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,湖北武汉430022
出 处:《中国神经免疫学和神经病学杂志》2006年第2期102-105,共4页Chinese Journal of Neuroimmunology and Neurology
基 金:国家自然科学基金资助项目(30300114)
摘 要:目的研究纹状体区神经生长因子诱导蛋白-β(NGFI-β)的表达变化在左旋多巴诱发的异动症(LID)形成中所起的作用。方法分别以SCH23390(D1受体拮抗剂)、氟哌啶醇(D2受体拮抗剂)治疗LID大鼠,观察LID大鼠的行为学改变并用逆转录聚合酶链反应技术检测其纹状体区NGFI-βmRNA表达的变化。结果SCH23390治疗后,LID大鼠异常不自主运动明显减少,而氟哌啶醇治疗后则无明显改变。氟哌啶醇治疗后纹状体NGFI-βmRNA的表达较治疗前明显增多,而SCH23390治疗后无明显改变。结论大鼠纹状体区NGFI-β基因的表达变化与LID的形成有关,直接通路活动异常及基底节环路功能异常参与大鼠LID的发生。Objective To study the expression of nerve growth factor inducible protein B gene (NGFI-β) in striatum in the pathogcnesis of levodopa-induced dyskinesias(LID), Methods The rat model of LID was treated with SCH 23390(dopamine D1 antagonist) and haloperido[ ( dopamine D2 antagonist) respectively. Reverse transcriptase- polymerasc chain reaction (RT-PCR) was used to measure the expressions of NGFI-β mRNA in striatum while the behavior changes were observed. Results After treatment with SCH23390, abnormal involuntary movement (AIM) in LII) rats was decreased and the changes of expression of NGFI-β mRNA in striatum were not significant. After treatment with halopcridol, the changes of AIM in LID rats were not significant and the expression of NGFI-β mRNA was increased significantly. Conclusions LID is associated with over expression of NGFI-β in striatum. Abnormal activity in the direct pathway and the basal ganglia circuit might be involved in the development of LID.
关 键 词:异动症 左旋多巴 帕金森病 神经生长因子诱导蛋白-β
分 类 号:R742.5[医药卫生—神经病学与精神病学]
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