Neuronal overexpression of antioxidants reduces sleep, suggesting a role for ROS in sleep regulation.

<p>(A) Neuronal overexpression of the antioxidant genes <i>SOD1</i> and <i>SOD2</i> reduced sleep by 10% (B, <i>p</i> < 0.05 compared to either control, <i>n</i> = 16–40 flies/genotype) and 16% (<i>p</i> < 0.01 compared to either control, <i>n</i> = 16–38 flies/genotype), respectively. Neuronal overexpression of catalase also reduced sleep, but the decrease was not statistically significant compared to the driver control (<i>p</i> > 0.05 compared to <i>elav</i> control, <i>p</i> < 0.001 compared to <i>catalase</i> control, <i>n</i> = 16–40 flies/genotype). Each data point represents average sleep in minutes/day measured across 5 days in an individual animal; data are shown as mean ± SEM. <i>p</i>-values were obtained by ordinary one-way ANOVA followed by a post hoc Tukey test when significance was detected. Pooled data from two independent experiments are shown. (B) Model: high ROS levels promote sleep, which in turn clears ROS to promote wake. Raw data from representative experiments are available in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2005206#pbio.2005206.s006" target="_blank">S1 Data</a>; raw data from all trials are available upon request. ROS, reactive oxygen species; <i>SOD</i>, <i>superoxide dismutase</i>.