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Nersesyan, Y., Demirkhanyan, L., & Cabezas-Bratesco, D. (2017). Oxytocin Modulates Nociception as an Agonist of Pain-Sensing TRPV1. Cell Reports, 21(6), 1681–1691. Added by: Dr. Enrique Feoli (25/11/2023, 15:56) Last edited by: Dr. Enrique Feoli (25/11/2023, 15:58) |
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| Resource type: Journal Article DOI: 10.1016/j.celrep.2017.10.063 ID no. (ISBN etc.): 2211-1247 BibTeX citation key: Nersesyan2017 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Oxytocin analgesia Creators: Cabezas-Bratesco, Demirkhanyan, Nersesyan Collection: Cell Reports |
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| Abstract |
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Oxytocin is a hormone with various actions. Oxytocin-containing parvocellular neurons project to the brainstem and spinal cord. Oxytocin release from these neurons suppresses nociception of inflammatory pain, the molecular mechanism of which remains unclear. Here, we report that the noxious stimulus receptor TRPV1 is an ionotropic oxytocin receptor. Oxytocin elicits TRPV1 activity in native and heterologous expression systems, regardless of the presence of the classical oxytocin receptor. In TRPV1 knockout mice, DRG neurons exhibit reduced oxytocin sensitivity relative to controls, and oxytocin injections significantly attenuate capsaicin-induced nociception in in vivo experiments. Furthermore, oxytocin potentiates TRPV1 in planar lipid bilayers, supporting a direct agonistic action. Molecular modeling and simulation experiments provide insight into oxytocin-TRPV1 interactions, which resemble DkTx. Together, our findings suggest the existence of endogenous regulatory pathways that modulate nociception via direct action of oxytocin on TRPV1, implying its analgesic effect via channel desensitization.
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Publisher: Elsevier
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