Knockout of PINK1 altered the neural connectivity of Drosophila dopamine PPM3 neurons at input and output sites
Authors:
- 6 August 2020
- journal article
- research article
- Published by Springer Nature in Invertebrate Neuroscience
- Vol. 20 (3) , 1-9
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
Funding Information
- National Natural Science Foundation of China (81701414)
This publication has 37 references indexed in Scilit:
- Function and Characteristics of PINK1 in MitochondriaOxidative Medicine and Cellular Longevity, 2013
- The Mitochondrial Na+/Ca2+ Exchanger Upregulates Glucose Dependent Ca2+ Signalling Linked to Insulin SecretionPLOS ONE, 2012
- PARK6 PINK1 mutants are defective in maintaining mitochondrial membrane potential and inhibiting ROS formation of substantia nigra dopaminergic neuronsBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2011
- Signal Propagation inDrosophilaCentral NeuronsThe Journal of Neuroscience, 2009
- Eight different types of dopaminergic neurons innervate the Drosophila mushroom body neuropil: anatomical and physiological heterogeneityFrontiers in Neural Circuits, 2009
- Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stressProceedings of the National Academy of Sciences, 2008
- Complex I deficiency in Parkinson's disease frontal cortexBrain Research, 2008
- Impaired dopamine release and synaptic plasticity in the striatum of PINK1 -deficient miceProceedings of the National Academy of Sciences, 2007
- Drosophila pink1 is required for mitochondrial function and interacts genetically with parkinNature, 2006
- Cholinergic Synaptic Transmission in AdultDrosophilaKenyon CellsIn SituJournal of Neuroscience, 2006