Rotenone-Induced Parkinsonism

采用Alzet微型泵向右颈静脉滴注鱼藤酮（0、1.5、2.0、2.5 mg/kg/d），持续4周。采用抗酪氨酸羟化酶和ct-synuclein抗体，通过自发运动活性、纹状体多巴胺含量和黑质纹状体神经元免疫组化评价黑质纹状体通路的损伤。鱼藤酮灌胃组大鼠体重的增加幅度明显小于灌胃组。各组生存率分别为100、90、80、45%。与对照组相比，2.5 mg组小鼠自发性活动在第3周明显减弱，但在第4周恢复正常。其他组在自发活动方面没有统计学上的显著变化。形态学评价无明显变化。我们得出结论，Betarbet等人（2000）最初报道的鱼藤酮模型基本上是不可靠的。

Rotenone (0, 1.5, 2.0, 2.5 mg/kg/day) was infused with Alzet minipumps into the right jugular vein for 4 weeks. The impairment of the nigrostriatal pathway was evaluated by spontaneous motor activities, striatal dopamine contents and immunohistochemistry of nigral and striatal neurons by using antibodies against tyrosine hydroxylase and ct-synuclein. The increase in the body weight of the rotenone-infused rats was significantly smaller than that of the vehicle-infused ones. The survival rate of each group was 100, 90, 80 and 45%, respectively. The spontaneous activities were significantly deceased in the 2.5 mg group as compared with the vehicle group at the 3rd week but returned normal at the 4th week. The other groups showed no statistically significant changes in the spontaneous activities. There were no significant changes in morphological evaluations. We conclude the rotenone model that was originally reported by Betarbet et al. (2000) to be substantially unreliable.