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Opiates modulate thermosensation by internalizing cold receptor TRPM8.

Authors
  • Bokhobza Alexandre
  • Shapovalov, George
  • Gkika, Dimitra
  • Devilliers, Maily
  • Kondratskyi, Artem
  • Gordienko, Dmitri
  • Busserolles, Jerome
  • Bokhobza, Alexandre
  • Eschalier, Alain
  • Skryma, Roman
  • Prevarskaya, Natalia
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Aug 14, 2013
Volume
4
Issue
3
Pages
504–515
Identifiers
DOI: 10.1016/j.celrep.2013.07.002
PMID: 23911290
Source
Medline
License
Unknown

Abstract

Stimulation of μ-opioid receptors (OPRMs) brings powerful pain relief, but it also leads to the development of tolerance and addiction. Ensuing withdrawal in abstinent patients manifests itself with severe symptoms, including cold hyperalgesia, often preventing addicted patients from successfully completing the rehabilitation. Unsurprisingly, OPRMs have been a central point of many studies. Nonetheless, a satisfactory understanding of the pathways leading to distorted sensory responses during opiate administration and abstinence is far from complete. Here, we present a mechanism that leads to modulation by OPRMs of one of the sensory responses, thermosensation. Activation of OPRM1 leads to internalization of a cold-sensor TRPM8, which can be reversed by a follow-up treatment with the inverse OPRM agonist naloxone. Knockout of TRPM8 protein leads to a decrease in morphine-induced cold analgesia. The proposed pathway represents a universal mechanism that is probably shared by regulatory pathways modulating general pain sensation in response to opioid treatment.

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