中文摘要：

客观：学习神经生长因素的表示的角色在在导致 levodopa 的运动障碍(盖) 的致病的条纹弦音器的可诱导的蛋白质 B 基因(NGFI-B ) 。方法：盖的老鼠模型与 SCH 23390 被对待(1 mg/kg ip，一个多巴胺 D1 对手) 并且 haloperidol (1 mg/kg ip，一个多巴胺 D2 对手) 分别地。Reversetranscriptase 聚合酶链反应(RT-PCR ) 被用来测量 NGFI-B mRNAin 条纹弦音器的表示，行为变化被观察。结果：在有 SCH23390 的处理以后，在盖老鼠的反常非自愿的运动(目的) 被减少(P 【 0.05 ) 并且 NGFI-B mRNAin 条纹弦音器的表示没显著地变化。在有 haloperidol 的处理以后，在盖老鼠的目的变化不是重要的， NGFI-B mRNA 的表示显著地被增加(P 【0.01 ) 。结论：盖在条纹弦音器与 NGFI-B 的在表示上被联系。在直接小径的反常活动并且基础轧了神经胶质电路能涉及盖的出现。

英文摘要：

Objective： To study the role of the expression of nerve growth factor inducible protein B gene （NGFI-B） in striatum in the pathogenesis of levodopa-induced dyskinesias （LID）. Methods： The rat model of LID was treated with SCH 23390（1 mg/kg ip,a dopamine D1 antagonist） and haloperidol （1 mg/kg ip,a dopanfme D2 antagonist） respectively. Reverse transcriptase-polymerase chain reaction （RT-PCR） was used to measure the expression of NGFI-B mRNA in stiiatam and the behavior changes were observed. Resuits： After treatment with SCH23390, abnormal involuntary movement （AIM） in LID rats was decreased （ P 〈 0.05 ） and the expression of NGFI-B mRNA in striatum did not change significantly. After treatment with haloperidol, the changes of AIM in LID rats were not significant and the expression of NGFI-B mRNA was increased significantly（ P 〈 0.01）. Conclusion： LID is associated with over-expression of NGFI-B in striatum. Abnormal activity in the direct pathway and the basal ganglia circuit could be involved in the occurrence of LID.