title: Sensory Neurons Arouse C. elegans Locomotion via Both Glutamate and Neuropeptide Release.
abstract: C. elegans undergoes periods of behavioral quiescence during larval molts (termed lethargus) and as adults. Little is known about the circuit mechanisms that establish these quiescent states. Lethargus and adult locomotion quiescence is dramatically reduced in mutants lacking the neuropeptide receptor NPR-1. Here, we show that the aroused locomotion of npr-1 mutants results from the exaggerated activity in multiple classes of sensory neurons, including nociceptive (ASH), touch sensitive (ALM and PLM), and stretch sensing (DVA) neurons. These sensory neurons accelerate locomotion via both neuropeptide and glutamate release. The relative contribution of these sensory neurons to arousal differs between larval molts and adults. Our results suggest that a broad network of sensory neurons dictates transitions between aroused and quiescent behavioral states.
authors.affiliation: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America; Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, United States of America; Biological and Biomedical Sciences program, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Seungwon
authors.initials: S
authors.lastname: Choi
authors.affiliation: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America; Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, United States of America; Biological and Biomedical Sciences program, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Kelsey P
authors.initials: KP
authors.lastname: Taylor
authors.affiliation: Cell Biology Division, MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
authors.forename: Marios
authors.initials: M
authors.lastname: Chatzigeorgiou
authors.affiliation: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America; Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Zhitao
authors.initials: Z
authors.lastname: Hu
authors.affiliation: Cell Biology Division, MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
authors.forename: William R
authors.initials: WR
authors.lastname: Schafer
authors.affiliation: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America; Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, United States of America; Biological and Biomedical Sciences program, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Kaplan
mesh_terms: D000818:Animals; D001143:Arousal / Q000502:physiology; D001522:Behavior, Animal / Q000502:physiology; D017173:Caenorhabditis elegans / Q000378:metabolism / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics*; D002465:Cell Movement / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism*; D009479:Neuropeptides / Q000378:metabolism*; D009619:Nociceptors / Q000378:metabolism; D017476:Receptors, Neuropeptide Y / Q000235:genetics*; D011984:Sensory Receptor Cells / Q000378:metabolism*; D012890:Sleep / Q000502:physiology
chemical_list: D029742:Caenorhabditis elegans Proteins; C468272:NPR-1 protein, C elegans; D009479:Neuropeptides; D017476:Receptors, Neuropeptide Y; D018698:Glutamic Acid