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Neuron. 2013 Jun 5;78(5):869-80. doi: 10.1016/j.neuron.2013.04.002.

Analysis of NPR-1 reveals a circuit mechanism for behavioral quiescence in C. elegans.

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1
Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.

Abstract

Animals undergo periods of behavioral quiescence and arousal in response to environmental, circadian, or developmental cues. During larval molts, C. elegans undergoes a period of profound behavioral quiescence termed lethargus. Locomotion quiescence during lethargus was abolished in mutants lacking a neuropeptide receptor (NPR-1) and was reduced in mutants lacking NPR-1 ligands (FLP-18 and FLP-21). Wild-type strains are polymorphic for the npr-1 gene, and their lethargus behavior varies correspondingly. Locomotion quiescence and arousal were mediated by decreased and increased secretion of an arousal neuropeptide (PDF-1) from central neurons. PDF receptors (PDFR-1) expressed in peripheral mechanosensory neurons enhanced touch-evoked calcium transients. Thus, a central circuit stimulates arousal from lethargus by enhancing the sensitivity of peripheral mechanosensory neurons in the body. These results define a circuit mechanism controlling a developmentally programmed form of quiescence.

PMID:
23764289
PMCID:
PMC3683153
DOI:
10.1016/j.neuron.2013.04.002
[Indexed for MEDLINE]
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