Neuropeptides are a class of neuromodulators that act on neural circuits to generate dynamic circuit properties and behavioral states. Neuropeptide circuit modulation is thought to generate behavioral states as varied as an "awake" and a "sleep" state. Sleep is classically defined as a state with behavioral quiescence, response latency (delayed response to sensory stimulus), and homeostatic regulation. By this definition, sleep has been observed in C. elegans, D. melanogaster, zebrafish, and mice, as well as humans. Three conditions induce sleep in C. elegans: developmental lethargus, epidermal growth factor (EGF)-, and satiety-induced sleep. Here we focus on EGF induced sleep. Stress, including temperature elevation, leads to EGF activation of the EGFR ortholog LET-23 in the peptidergic ALA neuron. To determine how ALA induces sleep, we profiled the transcriptome of this neuron and found that many neuropeptide encoding genes were highly expressed in ALA. We characterized the effect of four neuropeptides (FLP-13, FLP-24, NLP-8, and FLP-7) on five behaviors: feeding, defecation, locomotion, head movement, and response latency. Behavioral quiescence in C. elegans is typically assayed by cessation of eating and locomotion, but defecation ceases as well. We wanted to determine if neuropeptides modulate the defecation motor program (DMP) during sleep. We found that NLP-8 inhibits defecation, but not feeding, indicating that defecation is modulated independently of feeding. While some behaviors were exclusively modulated by one neuropeptide, other behaviors were modulated by several. These data suggest that EGF-ALA induced sleep occurs by partly independent neuropeptide modulation of eating, defecation, locomotion, and response latency, which together constitute much of the sleep state.
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