电针对帕金森模型型小鼠SNC突触多巴胺影响的调节作用研究
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摘要
目的:研究电针对帕金森模型小鼠黑质致密部突触多巴胺影响的调节作用。
     方法:以MPTP诱导的PD模型小鼠作为研究对象,电针“合谷”、“太冲”四关穴,每日1次,7次为1疗程,共3个疗程。观察造模前后PD模型小鼠的行为学表现,免疫组化检测电针前后黑质致密部多巴胺转运体、γ—氨基丁酸表达变化。
     结果:模型组小鼠有类似临床PD行为障碍的表现;电针组小鼠与模型组小鼠相比较,黑质致密部多巴胺转运体、γ—氨基丁酸表达增强。
     结论:电针具有调节PD模型小鼠黑质致密部突触多巴胺的作用;其机制可能与促进黑质致密部多巴胺转运体对多巴胺的再摄取、促进γ—氨基丁酸的兴奋性抑制有关。
Objective: To research on the content of dopamine neuron in substantia
    nigra zona compact in Parkinson' s disease model mouse treated by electroacupuncture therapy.
    Methods: The parkinson' s disease mouce induced by 1-methyl, 4-phenyl
    - 1, 2, 3, 6 tetrahydropyridine were treated by electroacupuncture therapy on "Hegu(LI4)" and "Taichong(LV3) " acupoints. The treatment was once daily and up to seven as one course which was lasted for 3 courses. Behavior medicine of mouse between the model-group and control-group; Immunohistochemistry for the exppresion of dopamine transporter and gamma-aminobutyric acid.
    Results: Model mouse perform behavior disturbance similar with
    clinical symptoms of Parkinson' s disease. Compared to model mouse, the expressions of transporter and gamma-aminobutyric acid were increased after electroacupuncture treatment.
    Conclusions: Electroacupuncture treatment for parkinson' s desease
    mouse can regulate the content of dopamine in synaptic cleft in substantia nigra zona compact. The mechanism is maybe due to improving dopamine reuptaking by dopamine transporter and excitatory inhibition caused by gamma-aminobutyric acid.
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