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NMDA receptor stimulation can lead to ROS generation ( Bindokas et al., 1996 Brennan et al., 2009 Dugan et al., 1995), and in hippocampal and spinal cord slices ROS have been shown sufficient and necessary for inducing ‘Hebbian’ forms of plasticity (LTP) ( Kamsler and Segal, 2003a Kamsler and Segal, 2003b Klann, 1998 Knapp and Klann, 2002 Lee et al., 2010). We previously showed in a model for lysosomal storage diseases that ROS can regulate neuromuscular junction (NMJ) structure ( Milton et al., 2011). Moreover, several kinase signaling pathways are enhanced by ROS, either by oxidation of kinase interacting modulators, such as thioredoxin or glutathione-S-transferases ( Adler et al., 1999 Saitoh et al., 1998), or through inhibition of counteracting phosphatases, for example PTEN, by oxidation of the active site cysteine residue ( Finkel, 2011 Stuart et al., 2014 Tonks, 2005). Importantly, ROS have also been recognized as signaling molecules in metabolic pathways ( Liemburg-Apers et al., 2015) and controlling the activity of transcription factors such as AP-1 and Nrf2 ( Jindra et al., 2004 Soriano et al., 2009).
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Implicit in their name, ROS are highly reactive, containing one or more unpaired electrons, with the potential to modify and damage by oxidation proteins, lipids and DNA ( Gladyshev, 2014 Harman, 1956 Stuart et al., 2014). Mitochondria are a significant source of ROS, which form as obligate byproducts of respiratory ATP synthesis by ‘leakage’ of the electron transport chain, thus leading to the generation of superoxide anions (O 2 -) and hydrogen peroxide (H 2O 2) ( Halliwell, 1992). Levels of reactive oxygen species (ROS) in the brain increase with ageing and high levels of ROS are a hallmark of neurodegeneration, including Alzheimer’s and Parkinson’s disease ( Höhn and Grune, 2013 Martins et al., 1986 Spina and Cohen, 1989) for review see ( Milton and Sweeney, 2012). 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. We identified the highly conserved Parkinson’s disease-linked protein DJ-1β as a redox sensor in neurons where it regulates structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway.
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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.
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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. Their role in the nervous system under non-pathological conditions has remained poorly understood. Reactive oxygen species (ROS) have been extensively studied as damaging agents associated with ageing and neurodegenerative conditions.
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