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 -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.
Identifer | oai:union.ndltd.org:harvard.edu/oai:dash.harvard.edu:1/11158244 |
Date | 08 June 2015 |
Creators | Choi, Seungwon |
Contributors | Kaplan, Joshua M. |
Publisher | Harvard University |
Source Sets | Harvard University |
Language | en_US |
Detected Language | English |
Type | Thesis or Dissertation |
Rights | open |
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