左旋多巴诱发异动症大鼠模型基底节区谷氨酸脱羧酶表达的研究

目的 研究左旋多巴诱发异动症(LID)大鼠模型尾壳核、苍白球及黑质网状部谷氨酸脱羧酶(GAD)表达的变化。方法用免疫组织化学方法观测大鼠尾壳核、苍白球及黑质网状部GAD的表达变化，用辣根过氧化物酶(HRP)逆行示踪与免疫组织化学相结合的双重反应技术观测GAD的细胞分布状况。结果 LID大鼠较正常及非LID大鼠尾壳核区GAD明显增加，尤其在尾壳核外侧区增加更明显，且主要分布在纹状体黑质神经元内，苍白球区GAD明显增加，而黑质网状部GAD减少。结论 大鼠基底节区GAD表达变化与LID的发生有关，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。

Expression of GAD in the basal ganglia of levodopa-induced dyskinesia in the rat

Objective To study the changes in expression of GAD in the caudate-putamen(CPU),globus pallidus(GP) and substantia nigra pars reticula (SNr) of levodopa-induced dyskinesia (LID) rat model.Methods Immunohistochemistry was used to measure changes in expression of GAD in the CPU,GP and SNr.Double labling technique including immunohistochemistry of GAD and retrograde HRP transport tracing was used to observe the cell distribution of GAD.Results In the LID rats,expression of GAD was significantly increased in the DA-denevated striatum compared with normal and non-LID rats,and an area of especially strong GAD epression was found in the lateral CPU,in addition,most cells expressed GAD were striatonigral neurons.Expression of GAD in the GP and SNr were increased and decreased,respectirely.Conclusions LID is associated with overexpression of GAD in the striatonigral neurons.Abnormal activity in the direct pathway and the basal ganglia circuit could involve in occurrence of LID.