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dc.contributor.authorRingstad, Niels
dc.contributor.authorAbe, Namiko
dc.contributor.authorHorvitz, Howard Robert
dc.date.accessioned2014-01-24T18:03:59Z
dc.date.available2014-01-24T18:03:59Z
dc.date.issued2009-07
dc.date.submitted2008-12
dc.identifier.issn0036-8075
dc.identifier.issn1095-9203
dc.identifier.urihttp://hdl.handle.net/1721.1/84506
dc.description.abstractBiogenic amines such as serotonin and dopamine are intercellular signaling molecules that function widely as neurotransmitters and neuromodulators. We have identified in the nematode Caenorhabditis elegans three ligand-gated chloride channels that are receptors for biogenic amines: LGC-53 is a high-affinity dopamine receptor, LGC-55 is a high-affinity tyramine receptor, and LGC-40 is a low-affinity serotonin receptor that is also gated by choline and acetylcholine. lgc-55 mutants are defective in a behavior that requires endogenous tyramine, which indicates that this ionotropic tyramine receptor functions in tyramine signaling in vivo. Our studies suggest that direct activation of membrane chloride conductances is a general mechanism of action for biogenic amines in the modulation of C. elegans behavior.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant GM24663)en_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.description.sponsorshipLife Sciences Research Foundationen_US
dc.description.sponsorshipMedical Foundation, Inc.en_US
dc.language.isoen_US
dc.publisherAmerican Association for the Advancement of Science (AAAS)en_US
dc.relation.isversionofhttp://dx.doi.org/10.1126/science.1169243en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourcePMCen_US
dc.titleLigand-Gated Chloride Channels Are Receptors for Biogenic Amines in C. elegansen_US
dc.typeArticleen_US
dc.identifier.citationRingstad, N., N. Abe, and H. R. Horvitz. “Ligand-Gated Chloride Channels Are Receptors for Biogenic Amines in C. elegans.” Science 325, no. 5936 (July 2, 2009): 96-100.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentMcGovern Institute for Brain Research at MITen_US
dc.contributor.mitauthorRingstad, Nielsen_US
dc.contributor.mitauthorAbe, Namikoen_US
dc.contributor.mitauthorHorvitz, H. Roberten_US
dc.relation.journalScienceen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsRingstad, N.; Abe, N.; Horvitz, H. R.en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-9964-9613
mit.licenseOPEN_ACCESS_POLICYen_US
mit.metadata.statusComplete


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