Reactive Oxygen Species Regulate Activity-Dependent Neuronal Plasticity in Drosophila

Matthew Charles William Oswald, Paul S. Brooks, Maarten F. Zwart, Amrita Mukherjee, Ryan John Hatcher West, Carlo Giachello, Khomgrit Morarach, Richard A. Baines, Sean Sweeney, Matthias Landgraf

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Reactive oxygen species (ROS) have been extensively studied as damaging agents associated with ageing and neurodegenerative conditions. Their role in the nervous system under non-pathological conditions has remained poorly understood. Working with the Drosophila larval locomotor network, we show that in neurons ROS act as obligate signals required for neuronal activity-dependent structural plasticity, of both pre- and postsynaptic terminals. ROS signaling is also necessary for maintaining evoked synaptic transmission at the neuromuscular junction, and for activity-regulated homeostatic adjustment of motor network output, as measured by larval crawling behavior. We identified the highly conserved Parkinson’s disease-linked protein DJ-1ß as a redox sensor in neurons where it regulates structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway. This study provides a new conceptual framework of neuronal ROS as second messengers required for neuronal plasticity and for network tuning, whose dysregulation in the ageing brain and under neurodegenerative conditions may contribute to synaptic dysfunction.
Original languageEnglish
Article numbere39393
Early online date12 Dec 2018
Publication statusPublished - 17 Dec 2018

Bibliographical note

© 2018, Oswald et al.

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