Promotion of behavior and neuronal function by reactive oxygen species in C. elegans.

Reactive oxygen species (ROS) are well known to elicit a plethora of detrimental effects on cellular functions by causing damages to proteins, lipids and nucleic acids. Neurons are particularly vulnerable to ROS, and nearly all forms of neurodegenerative diseases are associated with oxidative stress. Here, we report the surprising finding that exposing C. elegans to low doses of H(2)O(2) promotes, rather than compromises, sensory behavior and the function of sensory neurons such as ASH. This beneficial effect of H(2)O(2) is mediated by an evolutionarily conserved peroxiredoxin-p38/MAPK signaling cascade. We further show that p38/MAPK signals to AKT and the TRPV channel OSM-9, a sensory channel in ASH neurons. AKT phosphorylates OSM-9, and such phosphorylation is required for H(2)O(2)-induced potentiation of sensory behavior and ASH neuron function. Our results uncover a beneficial effect of ROS on neurons, revealing unexpected complexity of the action of oxidative stressors in the nervous system.