Knockout of PINK1 altered the neural connectivity of Drosophila dopamine PPM3 neurons at input and output sites
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ORIGINAL ARTICLE
Knockout of PINK1 altered the neural connectivity of Drosophila dopamine PPM3 neurons at input and output sites Jing‑Da Qiao1 · Yu‑Ling Mao2 Received: 4 February 2019 / Accepted: 9 July 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract 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. Keywords Parkinson disease · PINK1 · Electrophysiology
Introduction Parkinson disease (PD) is the second most common neurodegenerative disease in the world. Impaired ability in motor control of the body and cognitive decline are the major symptoms in PD patients which negatively influence the quality of life (Aarsland et al. 2017; Lang and Espay 2018; Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10158-020-00244-4) contains supplementary material, which is available to authorized users. * Yu‑Ling Mao [email protected] 1
Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University; Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China
Center for Reproductive Medicine, the Third Affiliated Hospital of Guangzhou Medical University; Key Laboratory for Reproductive Medicine of Guangdong; Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes; and Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, People’s Republic of China
2
Massano and Bhatia 2012; Poewe et al. 2017; RodriguezOroz et al. 2009). The reduction of the dopaminergic neurons in the midbrain substantia nigra by apoptosis leads to an insufficiency in dopamine release to the striatum (Dickson et al. 2009; Michel et al. 2016). The striatum is an important structure of motor and reward systems. The causes of dopamine neuron depletion by apoptosis in the substantia nigra are still unclear. Several authors reported that complex one activity was found to decrease in the substantia nigra in PD patients (Exner et al. 2012; Parker et
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