摘要：SummaryAnimals require robust yet flexible programs to support locomotion. Here we report a pathway that connects the D1-like dopamine receptor DOP-1 with a sleep mechanism to modulate swimming inC. elegans. We show that DOP-1 plays a negative role in sustaining swimming behavior. By contrast, a pathway through the D2-like dopamine receptor DOP-3 negatively regulates the initiation of swimming, but its impact fades quickly over a few minutes. We find that DOP-1 and the GPCR kinase (G-protein-coupled receptor kinase-2) function in the sleep interneuron RIS, where DOP-1 modulates the secretion of a sleep neuropeptide FLP-11. We further show that DOP-1 and FLP-11 act in the same pathway to modulate swimming. Together, these results delineate a functional connection between a dopamine receptor and a sleep program to regulate swimming inC. elegans. The temporal transition between DOP-3 and DOP-1 pathways highlights the dynamic nature of neuromodulation for rhythmic movements that persist over time.Graphical abstractDisplay OmittedHighlights•The D1-like dopamine receptor DOP-1 regulates swimming at 10 min•An integrated function of DOP-1 and DOP-3 is required for the continuity of swimming•DOP-1 and GRK-2 act in the sleep neuron RIS•FLP-11, a neuropeptide that promotes sleep, negatively regulates swimmingBiological Sciences ; Neuroscience ; Behavioral Neuroscience
