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34 reviewsSleep could protect animals from oxidative damage, yet the dynamic interplay between the redox state andsleep homeostasis remains unclear. Here, we show that acute sleep deprivation (SD) in mice caused a general increase in brain oxidation, particularly in sleep-promoting regions. In vivo imaging of intracellularhydrogen peroxide (H2O2) real-time dynamics revealed that in nigra sleep neurons, the increase in cytosolicbut not mitochondrial H2O2 reflects sleep debt and tracks spontaneous wakefulness by positively correlatingwith wake duration. By controllably manipulating intraneuronal H2O2, we discovered that H2O2 elevation isrequired for compensatory sleep and causally promotes sleep initiation, at least partly dependent on transient receptor potential melastatin 2 (TRPM2) channel. However, excessive H2O2 induced brain inflammationand sleep fragmentation. Together, our study demonstrates intraneuronal H2O2 as a crucial signalingmolecule that translates brain redox imbalance into sleep drive and underscores the significance of oxidativeeustress in sleep homeostasis.
