Abstract
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.
Author Summary Sleep behavior and survival benefits are independently regulated functions of the sleep neuron RIS in Caenorhabditis elegans.
Competing Interest Statement
The authors have declared no competing interest.
