中文摘要：

目的研究左旋多巴诱发异动症（LID）模型大鼠纹状体区特异性神经肽基因表达的变化,探讨LID时纹状体神经元的可塑性变化。方法分别以SCH23390（D1受体拮抗剂）和氟哌啶醇（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前脑啡肽原（PPE）及前强啡肽原（PDyn）基因的表达情况。结果LID大鼠经SCH23390治疗后,异常不自主运动（AIM）明显减少,其纹状体区PDyn mRNA表达量较LID组显著减少,PPE mRNA表达量无明显变化。经氟哌啶醇治疗后LID大鼠AIM无明显改变,其纹状体区PDyn mRNA和PPE mRNA表达量与LID组相比较均无明显变化。结论大鼠纹状体黑质神经元下游靶基因PDyn的表达异常与LID的形成有关,直接通路活动的异常增高和基底节环路功能异常参与了大鼠LID的形成。

英文摘要：

Objective To study the changes in the specific neuropeptide gene in the striatum of Levodopa-induced dyskinesia（LID） rat model, and to explore plasticity of striatal neurons in LID. Methods The rat model of LID was treated with SCH 23390（a dopamine D1 antagonist） and haloperidol （a dopamine D2 antagonist） respectively. Reverse transcriptase-polymerase chain reaction（RT-PCR） was used to detect the expression of preproenkephalin（PPE） and prodynorphin（PDyn） mRNA in striatum, and the behavior changes were observed. Results After treatment with SCH23390, abnormal involuntary movement （AIM） in LID rats was decreased, the expression of PDyn mRNA was decreased significantly and PPE mRNA had no change in striatum of 6-OHDA-lesioned hemisphere. After treatment with haloperidol, the changes of AIM in LID rats were not significant and the expression of PDyn mRNA and PPE mRNA had no significant change. Conclusion LID is associated with overexpression of specific gene PDyn on the direct pathway in striatum. Abnormal activity in the direct pathway and the basal ganglia circuit are involve in the occurrence of LID.