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Oxytocin Modulates Nociception as an Agonist of Pain-Sensing TRPV1.

Abstract：

: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.

journal_name

Cell Rep

journal_title

Cell reports

authors

Nersesyan Y,Demirkhanyan L,Cabezas-Bratesco D,Oakes V,Kusuda R,Dawson T,Sun X,Cao C,Cohen AM,Chelluboina B,Veeravalli KK,Zimmermann K,Domene C,Brauchi S,Zakharian E

doi

10.1016/j.celrep.2017.10.063

subject

Has Abstract

pub_date

2017-11-07 00:00:00

pages

1681-1691

issue

6

issn

2211-1247

pii

S2211-1247(17)31511-5

journal_volume

21

pub_type

杂志文章

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