Show simple item record

dc.contributor.authorIm, Seol Hee
dc.contributor.authorTakle, Kendra
dc.contributor.authorJo, Juyeon
dc.contributor.authorBabcock, Daniel T.
dc.contributor.authorMa, Zhiguo
dc.contributor.authorXiang, Yang
dc.contributor.authorGalko, Michael J.
dc.date2022-08-11T08:09:44.000
dc.date.accessioned2022-08-23T16:41:20Z
dc.date.available2022-08-23T16:41:20Z
dc.date.issued2015-11-17
dc.date.submitted2015-12-23
dc.identifier.citationElife. 2015 Nov 17;4. pii: e10735. doi: 10.7554/eLife.10735. <a href="http://dx.doi.org/10.7554/eLife.10735">Link to article on publisher's site</a>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.10735
dc.identifier.pmid26575288
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39864
dc.description<p>Co-author Kendra Takle is a student in the Neuroscience Program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractPain signaling in vertebrates is modulated by neuropeptides like Substance P (SP). To determine whether such modulation is conserved and potentially uncover novel interactions between nociceptive signaling pathways we examined SP/Tachykinin signaling in a Drosophila model of tissue damage-induced nociceptive hypersensitivity. Tissue-specific knockdowns and genetic mutant analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are required for damage-induced thermal nociceptive sensitization. Electrophysiological recording showed that DTKR99D is required in nociceptive sensory neurons for temperature-dependent increases in firing frequency upon tissue damage. DTKR overexpression caused both behavioral and electrophysiological thermal nociceptive hypersensitivity. Hedgehog, another key regulator of nociceptive sensitization, was produced by nociceptive sensory neurons following tissue damage. Surprisingly, genetic epistasis analysis revealed that DTKR function was upstream of Hedgehog-dependent sensitization in nociceptive sensory neurons. Our results highlight a conserved role for Tachykinin signaling in regulating nociception and the power of Drosophila for genetic dissection of nociception.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26575288&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>© 2015, Im et al. This article is distributed under the terms of the<a href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</a>permitting unrestricted use and redistribution provided that the original author and source are credited.</p>
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectDrosophila melanogaster
dc.subjectneuroscience
dc.subjectMolecular and Cellular Neuroscience
dc.titleTachykinin acts upstream of autocrine Hedgehog signaling during nociceptive sensitization in Drosophila
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume4
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3668&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2664
dc.identifier.contextkey7972047
refterms.dateFOA2022-08-23T16:41:21Z
html.description.abstract<p>Pain signaling in vertebrates is modulated by neuropeptides like Substance P (SP). To determine whether such modulation is conserved and potentially uncover novel interactions between nociceptive signaling pathways we examined SP/Tachykinin signaling in a Drosophila model of tissue damage-induced nociceptive hypersensitivity. Tissue-specific knockdowns and genetic mutant analyses revealed that both Tachykinin and Tachykinin-like receptor (DTKR99D) are required for damage-induced thermal nociceptive sensitization. Electrophysiological recording showed that DTKR99D is required in nociceptive sensory neurons for temperature-dependent increases in firing frequency upon tissue damage. DTKR overexpression caused both behavioral and electrophysiological thermal nociceptive hypersensitivity. Hedgehog, another key regulator of nociceptive sensitization, was produced by nociceptive sensory neurons following tissue damage. Surprisingly, genetic epistasis analysis revealed that DTKR function was upstream of Hedgehog-dependent sensitization in nociceptive sensory neurons. Our results highlight a conserved role for Tachykinin signaling in regulating nociception and the power of Drosophila for genetic dissection of nociception.</p>
dc.identifier.submissionpathoapubs/2664
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentYang Xiang Lab
dc.contributor.departmentNeurobiology
dc.contributor.studentKendra Takle Ruppell
dc.description.thesisprogramNeuroscience


Files in this item

Thumbnail
Name:
eLife.10735.full.pdf
Size:
7.138Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

<p>© 2015, Im et al. This article is distributed under the terms of the<a href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</a>permitting unrestricted use and redistribution provided that the original author and source are credited.</p>
Except where otherwise noted, this item's license is described as <p>© 2015, Im et al. This article is distributed under the terms of the<a href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</a>permitting unrestricted use and redistribution provided that the original author and source are credited.</p>