摘要
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。
Objective To seek the pathological mechanism of the Parkinson's didease, and to find the pathological basis of EAA-receptor antagonid on the disease.Methods The C57BL mice with the Parkinson's disease, which were reproduced by ip injection of MPTP, were administered with ketamine, a NMDA-receptor antagonist or Bicucullin, a GABA-receptor antagonist, and their behavioral, pathological and biochemical changes were carefully observed and analyzed.〖WTHX]Results Compared with the control group, the remarkable changes in those aforementioned imdexes were observed in group of Ketamine+MPTP, Bicucullin+MPTP, and MPTP. 〖WTHX]Conclusion The dccrcascd function of ccntral GABA ncrvcs aggravated the symptoms of the Parkinson's disease and NMDA-receptor antagonists might have a therapeutic effect on the disease.
出处
《济宁医学院学报》
1998年第3期8-10,共3页
Journal of Jining Medical University
基金
美国中华医学基金
