Author
Listed:
- Maïly Devilliers
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol)
- Jérôme Busserolles
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol)
- Stéphane Lolignier
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol)
- Emmanuel Deval
(Université de Nice Sophia Antipolis
CNRS, Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275
LabEx Ion Channel Science and Therapeutics)
- Vanessa Pereira
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol)
- Abdelkrim Alloui
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol)
- Marine Christin
(Université de Nice Sophia Antipolis
CNRS, Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275
LabEx Ion Channel Science and Therapeutics)
- Bruno Mazet
(Aix Marseille Université, CNRS, CRN2M UMR 7286)
- Patrick Delmas
(Aix Marseille Université, CNRS, CRN2M UMR 7286)
- Jacques Noel
(Université de Nice Sophia Antipolis
CNRS, Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275
LabEx Ion Channel Science and Therapeutics)
- Michel Lazdunski
(Université de Nice Sophia Antipolis
CNRS, Institut de Pharmacologie Moléculaire et Cellulaire, UMR 7275)
- Alain Eschalier
(Clermont Université, Université d’Auvergne, Pharmacologie fondamentale et clinique de la douleur
Inserm, U 1107, Neuro-Dol
CHU Clermont-Ferrand, Service de pharmacologie)
Abstract
Morphine is the gold-standard pain reliever for severe acute or chronic pain but it also produces adverse side effects that can alter the quality of life of patients and, in some rare cases, jeopardize the vital prognosis. Morphine elicits both therapeutic and adverse effects primarily through the same μ opioid receptor subtype, which makes it difficult to separate the two types of effects. Here we show that beneficial and deleterious effects of morphine are mediated through different signalling pathways downstream from μ opioid receptor. We demonstrate that the TREK-1 K+ channel is a crucial contributor of morphine-induced analgesia in mice, while it is not involved in morphine-induced constipation, respiratory depression and dependence—three main adverse effects of opioid analgesic therapy. These observations suggest that direct activation of the TREK-1 K+ channel, acting downstream from the μ opioid receptor, might have strong analgesic effects without opioid-like adverse effects.
Suggested Citation
Maïly Devilliers & Jérôme Busserolles & Stéphane Lolignier & Emmanuel Deval & Vanessa Pereira & Abdelkrim Alloui & Marine Christin & Bruno Mazet & Patrick Delmas & Jacques Noel & Michel Lazdunski & Al, 2013.
"Activation of TREK-1 by morphine results in analgesia without adverse side effects,"
Nature Communications, Nature, vol. 4(1), pages 1-9, December.
Handle:
RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3941
DOI: 10.1038/ncomms3941
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