Sleep is a state of behavioral quiescence that is closely associated with survival. Sleep-active neurons promote sleep and survival. It is not known, however, whether sleep-active neurons need to cause sleep to promote survival. Here, we tested how depolarization of the sleep-active RIS neuron in Caenorhabditis elegans controls sleep and survival during larval starvation. Survival always increased with raised RIS depolarization. RIS depolarization promoted sleep over a long range. Unexpectedly, however, high levels of RIS depolarization caused a nearly complete loss of sleep. Similarly, overexpression of sleep-inducing FLP-11 neuropeptides in RIS inhibited sleep, indicating that overactive transmission from RIS inhibits sleep. Despite the loss of sleep, survival was normal following FLP-11 overexpression. Thus, RIS overactivation abolishes sleep yet supports survival. These results indicate that regulation of sleep and survival are separable functions of a sleep-active neuron that are normally coupled but can be uncoupled by sleep-neuron over activation.
Sleep behavior and survival benefits are independently regulated functions of the sleep neuron RIS in Caenorhabditis elegans .