环境毒素与帕金森病（PD）发病的关联性已在部分农药中得到证实。多巴胺能（DA）神经元选择性丢失是PD的重要病理特点，DAT在部分环境毒素诱发DA能神经元丢失中发挥重要作用。我们前期工作以一例存在农药甲氰菊酯（Fen）暴露史的特殊PD患者为线索，在离体及在体水平证实Fen与PD发病相关，然而其发病机制尚未明确。我们前期研究进一步发现Fen上调DAT的表达，据此我们推测DAT在Fen诱发的多巴胺能神经元损伤中发挥重要作用。本研究拟于离体和在体水平观察DAT在Fen介导的多巴胺神经元损伤中的作用及相关机制，从而为环境毒素诱发PD的发病机制研究提供新的证据。

Environmental factors have been reported to be correlated to the pathogenesis of Parkinson’s disease (PD). The hallmark pathology of PD is the progressive degeneration of dopaminergic neurons. Dopamine transporter (DAT) plays an important role in mediating the dopaminergic neurotoxicity induced by environmental toxins. We have found a patient suffered from PD after fenpropathrin (Fen, a newly pyrethroid) exposure in our clinic center, and we have found Fen could minic the pathogenesis and pathology feature of PD. However, the pathogenesis of Fen induced dopaminergic neurons loss is unclear. In our previous study, we found Fen upregulated the expression of dopamine transporter, so we speculate that dopamine transporter might exert an important role in Fen induced dopaminergic neurotoxicity. In this study, the role of dopamine transporter in regulating Fen induced neurotoxicity will be assessed, furthermore, underline mechanism of Fen regulate DAT will be explored. Finding from the research will help updating the recognization of the pathogenesis of PD.