Höglinger G U, Oertel W H, Hirsch E C
INSERM U679, Hopital de la Salpetriere, Paris, France.
J Neural Transm Suppl. 2006(70):269-72. doi: 10.1007/978-3-211-45295-0_41.
Treatment of rats with rotenone has been proposed in the year 2000 to provide an animal model of idiopathic Parkinson's disease. We review here the experience that has been gained meanwhile with this model. The published data suggest that the model does not ideally reproduce the pathophysiology of Parkinson's disease, that Rotenone treatment does not cause a purely neurodegenerative concondition, that the Rotenone model does not ideally recapitulate the motor symptoms of Parkinson's disease, that degeneration of the dopaminergic neurons is highly variable, that striatal neurons appear to degenerate more consistently than neurons in the substantia nigra, and that cytoplasmic accumulation of the tau protein is more abundant than alpha-synuclein aggregation in severely lesioned animals. In summary, these data suggest that Rotenone-treated rats model atypical Parkinsonism rather than idiopathic Parkinson's disease.
2000年有人提出用鱼藤酮处理大鼠来建立特发性帕金森病的动物模型。我们在此回顾一下在此期间通过该模型所获得的经验。已发表的数据表明，该模型并不能理想地重现帕金森病的病理生理学，鱼藤酮处理不会导致纯粹的神经退行性疾病状态，鱼藤酮模型不能理想地概括帕金森病的运动症状，多巴胺能神经元的变性差异很大，纹状体神经元似乎比黑质中的神经元变性更一致，并且在严重受损的动物中，tau蛋白的细胞质积累比α-突触核蛋白聚集更丰富。总之，这些数据表明，用鱼藤酮处理的大鼠模型模拟的是非典型帕金森综合征而非特发性帕金森病。
