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目的:观察左旋多巴诱发异动症(LID)大鼠模型缝隙连接蛋白36(CX36)表达,初步探讨缝隙连接在LID形成机制中的作用。方法:制备帕金森病(PD)和LID大鼠模型,将实验动物分3组:LID模型组、PD未治疗组、正常对照组。各组大鼠分2亚组(缝隙连接阻断剂处理组和生理盐水对照组),观察系统途径给予缝隙连接阻断剂甘珀酸(carbenoxolone)对各组大鼠不自主运动行为的影响。利用免疫组化法检测各组大鼠脑皮层运动区和纹状体区CX36表达并进行分析比较。结果:腹腔注射缝隙连接阻断剂甘珀酸对阿扑吗啡诱导的LID不自主运动和PD旋转行为均无明显影响(P>0.05)。免疫组化结果显示LID组皮层运动区和纹状体区CX36表达较PD组和正常组均有显著增多(P<0.05),PD组与正常对照组亦有明显差别(P<0.05)。结论:LID大鼠基底节及大脑皮层CX36表达增加,缝隙连接可能参与了LID的形成机制。
Objective: To observe the expression of connexin 36 (CX36) in the rat model of LID induced by L-dopa and to explore the role of gap junctions in the formation of LID. Methods: Parkinson’s disease (PD) and LID rat models were prepared. The experimental animals were divided into 3 groups: LID model group, PD untreated group and normal control group. Rats in each group were divided into 2 subgroups (gap junction blocker and saline control groups), and the effect of systemic administration of carbenoxolone, a gap junction blocker, on the involuntary movement of rats in each group was observed. Immunohistochemistry was used to detect CX36 expression in motor and striatum of cerebral cortex of rats in each group. RESULTS: Intraperitoneal injection of the gap junction blocker carbenicol had no effect on apomorphine-induced involuntary LID movement and PD rotation (P> 0.05). The results of immunohistochemistry showed that CX36 expression in cortex and striatum of LID group was significantly higher than that of PD group and normal group (P <0.05), PD group and normal control group were also significantly different (P <0.05). Conclusion: The expression of CX36 in basal ganglia and cerebral cortex of LID rats increased, and the gap junction may be involved in the mechanism of LID formation.