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dc.contributor.authorRowan, MP
dc.contributor.authorBierbower, SM
dc.contributor.authorEskander, MA
dc.contributor.authorSzteyn, K
dc.contributor.authorPor, ED
dc.contributor.authorGomez, R
dc.contributor.authorVeldhuis, N
dc.contributor.authorBunnett, NW
dc.contributor.authorJeske, NA
dc.date.accessioned2021-02-04T01:26:53Z
dc.date.available2021-02-04T01:26:53Z
dc.date.issued2014-04-02
dc.identifierpii: PONE-D-14-01250
dc.identifier.citationRowan, M. P., Bierbower, S. M., Eskander, M. A., Szteyn, K., Por, E. D., Gomez, R., Veldhuis, N., Bunnett, N. W. & Jeske, N. A. (2014). Activation of Mu Opioid Receptors Sensitizes Transient Receptor Potential Vanilloid Type 1 (TRPV1) via beta-Arrestin-2-Mediated Cross-Talk. PLOS ONE, 9 (4), https://doi.org/10.1371/journal.pone.0093688.
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11343/259365
dc.description.abstractThe transient receptor potential family V1 channel (TRPV1) is activated by multiple stimuli, including capsaicin, acid, endovanilloids, and heat (>42C). Post-translational modifications to TRPV1 result in dynamic changes to the sensitivity of receptor activation. We have previously demonstrated that β-arrestin2 actively participates in a scaffolding mechanism to inhibit TRPV1 phosphorylation, thereby reducing TRPV1 sensitivity. In this study, we evaluated the effect of β-arrestin2 sequestration by G-protein coupled receptors (GPCRs) on thermal and chemical activation of TRPV1. Here we report that activation of mu opioid receptor by either morphine or DAMGO results in β-arrestin2 recruitment to mu opioid receptor in sensory neurons, while activation by herkinorin does not. Furthermore, treatment of sensory neurons with morphine or DAMGO stimulates β-arrestin2 dissociation from TRPV1 and increased sensitivity of the receptor. Conversely, herkinorin treatment has no effect on TRPV1 sensitivity. Additional behavioral studies indicate that GPCR-driven β-arrestin2 sequestration plays an important peripheral role in the development of thermal sensitivity. Taken together, the reported data identify a novel cross-talk mechanism between GPCRs and TRPV1 that may contribute to multiple clinical conditions.
dc.languageEnglish
dc.publisherPUBLIC LIBRARY SCIENCE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleActivation of Mu Opioid Receptors Sensitizes Transient Receptor Potential Vanilloid Type 1 (TRPV1) via beta-Arrestin-2-Mediated Cross-Talk
dc.typeJournal Article
dc.identifier.doi10.1371/journal.pone.0093688
melbourne.affiliation.departmentPharmacology and Therapeutics
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titlePLoS One
melbourne.source.volume9
melbourne.source.issue4
dc.rights.licenseCC BY
melbourne.elementsid1210540
melbourne.contributor.authorBunnett, Nigel
dc.identifier.eissn1932-6203
melbourne.accessrightsOpen Access


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