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目的为研究帕金森氏病的发病机理及兴奋性氨基酸受体拮抗剂对帕金森氏病的防治提供实验资料。方法采用ＭＰＴＰ腹腔注射建立Ｃ５７ＢＬ小黑鼠帕金森氏病模型的过程中，同时用兴奋性氨基酸ＮＭＤＡ受体拮抗剂Ｋｅｔａｍｉｎｅ和ＧＡＢＡ受体拮抗剂Ｂｉｃｕｃｕｌｉｎ，观察其行为药理学变化。结果Ｋｅｔａｍｉｎｅ＋ＭＰＴＰ组和Ｂｉｃｕｃｕｌｉｎ＋ＭＰＴＰ组及ＭＰＴＰ组和生理盐水组比较，行为药理学指标都有明显改变。结论ＮＭＤＡ受体拮抗剂对小鼠帕金森氏病模型具有防治作用，ＧＡＢＡ神经元的功能降低可加重帕金森氏病的症状。
Objective To study the pathogenesis of Parkinson’s disease and excitatory amino acid receptor antagonists to provide experimental data on the prevention and treatment of Parkinson’s disease. Methods The intraperitoneal injection of MPTP was used to establish Parkinson’s disease model of C57BL mice. Ketamine, an excitatory amino acid NMDA receptor antagonist, and Bicuculin, a GABA receptor antagonist, were also used to observe the behavioral and pharmacological changes. Results The Ketamine + MPTP group, the Bicuculin + MPTP group, the MPTP group and the saline group had significant changes in behavioral and pharmacological parameters. Conclusion NMDA receptor antagonist can prevent and treat Parkinson ’s disease in mice. Decreased function of GABA neurons may aggravate the symptoms of Parkinson’ s disease.