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.
journal_name
Cell Repjournal_title
Cell reportsauthors
Shapovalov G,Gkika D,Devilliers M,Kondratskyi A,Gordienko D,Busserolles J,Bokhobza A,Eschalier A,Skryma R,Prevarskaya Ndoi
10.1016/j.celrep.2013.07.002subject
Has Abstractpub_date
2013-08-15 00:00:00pages
504-15issue
3issn
2211-1247pii
S2211-1247(13)00349-5journal_volume
4pub_type
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