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dc.contributor.authorGu, Pengyu
dc.contributor.authorWang, Fei
dc.contributor.authorShang, Ye
dc.contributor.authorLiu, Jingjing
dc.contributor.authorGong, Jiaxin
dc.contributor.authorXie, Wei
dc.contributor.authorHan, Junhai
dc.contributor.authorXiang, Yang
dc.date2022-08-11T08:08:34.000
dc.date.accessioned2022-08-23T15:59:43Z
dc.date.available2022-08-23T15:59:43Z
dc.date.issued2022-03-16
dc.date.submitted2022-05-05
dc.identifier.citation<p>Gu P, Wang F, Shang Y, Liu J, Gong J, Xie W, Han J, Xiang Y. Nociception and hypersensitivity involve distinct neurons and molecular transducers in <em>Drosophila</em>. Proc Natl Acad Sci U S A. 2022 Mar 22;119(12):e2113645119. doi: 10.1073/pnas.2113645119. Epub 2022 Mar 16. PMID: 35294287; PMCID: PMC8944580. <a href="https://doi.org/10.1073/pnas.2113645119">Link to article on publisher's site</a></p>
dc.identifier.issn0027-8424 (Linking)
dc.identifier.doi10.1073/pnas.2113645119
dc.identifier.pmid35294287
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30733
dc.description.abstractSignificance: Functional plasticity of the nociceptive circuit is a remarkable feature and is of clinical relevance. As an example, nociceptors lower their threshold upon tissue injury, a process known as allodynia that would facilitate healing by guarding the injured areas. However, long-lasting hypersensitivity could lead to chronic pain, a debilitating disease not effectively treated. Therefore, it is crucial to dissect the mechanisms underlying basal nociception and nociceptive hypersensitivity. In both vertebrate and invertebrate species, conserved transient receptor potential (Trp) channels are the primary transducers of noxious stimuli. Here, we provide a precedent that in Drosophila larvae, heat sensing in the nociception and hypersensitivity states is mediated by distinct heat-sensitive neurons and TrpA1 alternative isoforms.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=35294287&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2022 the Author(s). Published by PNAS. This article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectDrosophila
dc.subjectalternative splicing
dc.subjectnociception
dc.subjectnociceptive hypersensitivity
dc.subjecttransient receptor potential (Trp)
dc.subjectNeuroscience and Neurobiology
dc.titleNociception and hypersensitivity involve distinct neurons and molecular transducers in Drosophila
dc.typeArticle
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume119
dc.source.issue12
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3237&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/2204
dc.identifier.contextkey29018212
refterms.dateFOA2022-08-23T15:59:43Z
html.description.abstract<p>Significance: Functional plasticity of the nociceptive circuit is a remarkable feature and is of clinical relevance. As an example, nociceptors lower their threshold upon tissue injury, a process known as allodynia that would facilitate healing by guarding the injured areas. However, long-lasting hypersensitivity could lead to chronic pain, a debilitating disease not effectively treated. Therefore, it is crucial to dissect the mechanisms underlying basal nociception and nociceptive hypersensitivity. In both vertebrate and invertebrate species, conserved transient receptor potential (Trp) channels are the primary transducers of noxious stimuli. Here, we provide a precedent that in Drosophila larvae, heat sensing in the nociception and hypersensitivity states is mediated by distinct heat-sensitive neurons and TrpA1 alternative isoforms.</p>
dc.identifier.submissionpathfaculty_pubs/2204
dc.contributor.departmentYang Xiang Lab
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentDepartment of Neurobiology
dc.source.pagese2113645119


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Copyright © 2022 the Author(s). Published by PNAS. This article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).
Except where otherwise noted, this item's license is described as Copyright © 2022 the Author(s). Published by PNAS. This article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).