Figure 7.

Model for Hyperoxia-Dependent Locomotor Arousal from Multiple Sleep States

Behavioral quiescence during DTS and cellular stress-induced sleep (SIS) are initiated by different cues and mediated by distinct signaling pathways. During SIS, neuropeptides released by the ALA interneuron promote multiple sleep-associated behaviors, including reduced locomotion, head movement, feeding, defecation, and sensory responsiveness. It is not clear if a global sleep-promoting cell plays a similar role during DTS, but head movement quiescence in both states is dependent on the RIS interneuron. Locomotor quiescence in both DTS and SIS is rapidly reversed by hyperoxia when NPR-1 activity is low, suggesting that these sleep states also utilize a common effector of locomotor quiescence (blue arrow). Wild C. elegans isolates thrive in reduced-oxygen environments such as the inside of decomposing fruit, and hyperoxia is an indicator of surface exposure. Activation of oxygen-sensing neurons leads to secretion of arousal signals that override locomotor quiescence and allow escape. This oxygen-responsive plasticity in sleep is masked when NPR-1 activity is high (shown in red).