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目的为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理论根据。方法本实验采用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，观察其帕金森行为症状、病理变化及生化改变。结果Ｋｅｔａｍｉｎｅ＋ＭＰＴＰ组和Ｂｉｃｕｃｕｌｉｎ＋ＭＰＴＰ组及ＭＰＴＰ级和生理盐水组比较，上述指标都有明显改变。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
The purpose is to provide theoretical basis for the pathogenesis of Parkinson’s disease and excitatory amino acid receptor antagonists for prevention and treatment of Parkinson’s disease. Methods In this experiment, 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 used to observe the behavioral symptoms and pathological changes of Parkinson’s disease. Biochemical changes. Results The Ketamine + MPTP group and Bicuculin + MPTP group compared with MPTP group and saline group, the above indicators have significant changes. Conclusions NMDA receptor antagonist can prevent and treat Parkinson’s disease in mice and the function of GABA neurons may aggravate the symptoms of Parkinson’s disease