par Laurent, Patrick 
;Becker, Jérôme ;Valverde, Olga;Ledent, Catherine ;de Kerchove d'Exaerde, Alban ;Schiffmann, Serge N. ;Maldonado, Rafael;Vassart, Gilbert ;Parmentier, Marc
Référence Nature neuroscience, 8, 12, page (1735-1741)
Publication Publié, 2005-12
;Becker, Jérôme ;Valverde, Olga;Ledent, Catherine ;de Kerchove d'Exaerde, Alban ;Schiffmann, Serge N. ;Maldonado, Rafael;Vassart, Gilbert ;Parmentier, Marc Référence Nature neuroscience, 8, 12, page (1735-1741)
Publication Publié, 2005-12
Article révisé par les pairs
| Résumé : | Prolactin-releasing peptide (PrRP) and its receptor G protein-coupled receptor 10 (GPR10) are expressed in brain areas involved in the processing of nociceptive signals. We investigated the role of this new neuropeptidergic system in GPR10-knockout mice. These mice had higher nociceptive thresholds and stronger stress-induced analgesia than wild-type mice, differences that were suppressed by naloxone treatment. In addition, potentiation of morphine-induced antinociception and reduction of morphine tolerance were observed in mutants. Intracerebroventricular administration of PrRP in wild-type mice promoted hyperalgesia and reversed morphine-induced antinociception. PrRP administration had no effect on GPR10-mutant mice, showing that its effects are mediated by GPR10. Anti-opioid effects of neuropeptide FF were found to require a functional PrRP-GPR10 system. Finally, GPR10 deficiency enhanced the acquisition of morphine-induced conditioned place preference and decreased the severity of naloxone-precipitated morphine withdrawal syndrome. Altogether, our data identify the PrRP-GPR10 system as a new and potent negative modulator of the opioid system. |
