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dc.contributor.authorOkine, Bright N.
dc.contributor.authorMadasu, Manish K.
dc.contributor.authorMcGowan, Fiona
dc.contributor.authorPrendergast, Charles
dc.contributor.authorGaspar, Jessica C.
dc.contributor.authorHarhen, Brendan
dc.contributor.authorRoche, Michelle
dc.contributor.authorFinn, David P.
dc.date.accessioned2019-04-01T10:25:51Z
dc.date.available2019-04-01T10:25:51Z
dc.date.issued2016-12
dc.identifier.citationOkine, Bright N., Madasu, Manish K., McGowan, Fiona, Prendergast, Charles, Gaspar, Jessica C., Harhen, Brendan, Roche, Michelle, Finn, David P. (2016). N-palmitoylethanolamide in the anterior cingulate cortex attenuates inflammatory pain behaviour indirectly via a CB1 receptor-mediated mechanism. PAIN, 157(12), 2687-2696. doi: 10.1097/j.pain.0000000000000687en_IE
dc.identifier.issn0304-3959
dc.identifier.issn1872-6623
dc.identifier.urihttp://hdl.handle.net/10379/15083
dc.description.abstractThe neural substrates and mechanisms mediating the antinociceptive effects of the endogenous bioactive lipid, N-palmitoylethanolamide (PEA), require further investigation. We investigated the effects of exogenous PEA administration into the anterior cingulate cortex (ACC), an important brain region linked with cognitive and affective modulation of pain, on formalin-evoked nociceptive behaviour in rats. Potential involvement of peroxisome proliferator-activated receptor isoforms (PPAR) a and g or endocannabinoid-mediated entourage effects at cannabinoid(1) (CB1) receptors or transient receptor potential subfamily V member 1 (TRPV1) in mediating the effects of PEA was also investigated. Intra-ACC administration of PEA significantly attenuated the first and early second phases of formalin-evoked nociceptive behaviour. This effect was attenuated by the CB1 receptor antagonist AM251, but not by the PPAR alpha antagonist GW6471, the PPAR gamma antagonist GW9662, or the TRPV1 antagonist 5'-iodo resiniferatoxin. All antagonists, administered alone, significantly reduced formalin-evoked nociceptive behaviour, suggesting facilitatory/permissive roles for these receptors in the ACC in inflammatory pain. Post-mortem tissue analysis revealed a strong trend for increased levels of the endocannabinoid anandamide in the ACC of rats that received intra-ACC PEA. Expression of c-Fos, a marker of neuronal activity, was significantly reduced in the basolateral nucleus of the amygdala, but not in the central nucleus of the amygdala, the rostral ventromedial medulla or the dorsal horn of the spinal cord. In conclusion, these data indicate that PEA in the ACC can reduce inflammatory pain-related behaviour, possibly via AEA-induced activation of CB1 receptors and associated modulation of neuronal activity in the basolateral amygdala.en_IE
dc.description.sponsorshipThis work was funded by a Principal Investigator Programme Grant from Science Foundation Ireland (10/IN.1/B2976), a PhD fellowship to JCG from Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brazil (207530/2014-9), and a PhD Fellowship to MKM from the College of Science, NUI Galway.en_IE
dc.formatapplication/pdfen_IE
dc.language.isoenen_IE
dc.publisherLippincott, Williams & Wilkinsen_IE
dc.relation.ispartofPainen
dc.subjectFATTY-ACID AMIDEen_IE
dc.subjectPREFRONTAL CORTEXen_IE
dc.subjectESCAPE/AVOIDANCE BEHAVIORen_IE
dc.subjectCANNABINOID RECEPTORen_IE
dc.subjectNEUROPATHIC PAINen_IE
dc.subjectNOXIOUS STIMULIen_IE
dc.subjectRAT-BRAINen_IE
dc.subjectANANDAMIDEen_IE
dc.subjectAMYGDALAen_IE
dc.subjectMODELen_IE
dc.titleN-palmitoylethanolamide in the anterior cingulate cortex attenuates inflammatory pain behaviour indirectly via a CB1 receptor-mediated mechanismen_IE
dc.typeArticleen_IE
dc.date.updated2019-03-27T23:00:19Z
dc.identifier.doi10.1097/j.pain.0000000000000687
dc.local.publishedsourcehttps://dx.doi.org/ 10.1097/j.pain.0000000000000687en_IE
dc.description.peer-reviewedpeer-reviewed
dc.contributor.funderScience Foundation Irelanden_IE
dc.contributor.funderConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brazilen_IE
dc.contributor.funderCollege of Science, National University of Ireland, Galwayen_IE
dc.internal.rssid12477413
dc.local.contactDavid Finn, Dept. Of Pharmacology &, Therapeutics, Nui, Galway. 5280 Email: david.finn@nuigalway.ie
dc.local.copyrightcheckedYes
dc.local.versionACCEPTED
dcterms.projectinfo:eu-repo/grantAgreement/SFI/SFI Principal Investigator Programme (PI)/10/IN.1/B2976/IE/The role of the endocannabinoid system in anxiety-induced modulation of pain: sites and mechanisms of action/en_IE
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