Impairment of the dopamine system is the main cause of Parkinson disease (PD). PTEN-induced kinase 1 (PINK1) is possibly involved in pathogenesis of PD. However, its role in dopaminergic neurons has not been fully established yet. In the present investigation, we have used the PINK1 knockout Drosophila model to explore the role of PINK1 in dopaminergic neurons. Electrophysiological and behavioral tests indicated that PINK1 elimination enhances the neural transmission from the presynaptic part of dopaminergic neurons in the protocerebral posterior medial region 3 (PPM3) to PPM3 neurons (which are homologous to those in the substantia nigra in humans). Firing properties of the action potential in PPM3 neurons were also altered in the PINK1 knockout genotypes. Abnormal motor ability was also observed in these PINK1 knockout animals. Our results indicate that knockout of PINK1 could alter both the input and output properties of PPM3 neurons.

中文翻译：

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敲除PINK1会改变果蝇多巴胺PPM3神经元在输入和输出位点的神经连通性。

多巴胺系统受损是帕金森氏病（PD）的主要原因。PTEN诱导的激酶1（PINK1）可能与PD的发病机制有关。然而，其在多巴胺能神经元中的作用尚未完全确立。在本研究中，我们使用了PINK1基因敲除的果蝇该模型探索PINK1在多巴胺能神经元中的作用。电生理和行为测试表明，消除PINK1可以增强从大脑后后内侧3区（PPM3）到PPM3神经元（与人类黑质中的神经元同源）的多巴胺能神经元突触前部分的神经传递。在PINK1基因敲除基因型中，PPM3神经元中动作电位的发射特性也发生了变化。在这些PINK1基因敲除动物中也观察到异常的运动能力。我们的结果表明，敲除PINK1可能会改变PPM3神经元的输入和输出属性。