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dc.contributor.authorAnand, Uma
dc.contributor.authorOtto, William R
dc.contributor.authorSanchez-Herrera, Daniel
dc.contributor.authorFacer, Paul
dc.contributor.authorYiangou, Yiangos
dc.contributor.authorKorchev, Yuri
dc.contributor.authorBirch, Rolfe
dc.contributor.authorBenham, Christopher
dc.contributor.authorBountra, Chas
dc.contributor.authorChessell, Iain P
dc.contributor.authorAnand, Praveen
dc.date.accessioned2012-05-21T14:56:34Z
dc.date.available2012-05-21T14:56:34Z
dc.date.issued2008
dc.identifier.citationAnand , U , Otto , W R , Sanchez-Herrera , D , Facer , P , Yiangou , Y , Korchev , Y , Birch , R , Benham , C , Bountra , C , Chessell , I P & Anand , P 2008 , ' Cannabinoid receptor CB2 localisation and agonist-mediated inhibition of capsaicin responses in human sensory neurons ' , Pain , vol. 138 , no. 3 , pp. 667-80 . https://doi.org/10.1016/j.pain.2008.06.007
dc.identifier.issn1872-6623
dc.identifier.otherPURE: 561503
dc.identifier.otherPURE UUID: 559327f4-cebd-40a9-8b3c-62829f9e3652
dc.identifier.otherPubMed: 18692962
dc.identifier.otherScopus: 50349097911
dc.identifier.urihttp://hdl.handle.net/2299/8541
dc.description.abstractCannabinoid receptor 2 (CB2) agonists provide the potential for treating chronic pain states without CNS effects associated with CB1 receptor activation. Animal models suggest that they act mainly via non-neuronal cells, possibly inhibition of inflammatory cells in the periphery or CNS, or via release of beta-endorphin; however, the clinical relevance and mechanism of analgesic action is uncertain. Here, we demonstrate colocalisation of CB2 with CB1 and the capsaicin receptor TRPV1 in human dorsal root ganglion (DRG) sensory neurons and increased levels of CB2 receptors in human peripheral nerves after injury, particularly painful neuromas. In primary cultures of human DRG neurons, selective CB2 agonists blocked activation of inward cation currents and elevation of cytoplasmic Ca2+ in response to capsaicin. These inhibitory effects were reversed by GW818646X a CB2 antagonist, and 8-bromo cAMP, but not by SR141716 a CB1 antagonist, or naloxone. Thus CB2 receptor agonists functionally inhibited nociceptive signalling in human primary sensory neurons via a mechanism shared with opioids, of adenylyl cyclase inhibition, but not via mu-opioid receptors. We conclude that CB2 agonists deserve imminent clinical trials for nociceptive, inflammatory and neuropathic chronic pain, in which capsaicin or heat-activated responses via TRPV1 may provide a clinical marker.en
dc.format.extent14
dc.language.isoeng
dc.relation.ispartofPain
dc.subjectAdolescent
dc.subjectAdult
dc.subjectAged
dc.subjectAnimals
dc.subjectCHO Cells
dc.subjectCannabinoids
dc.subjectCapsaicin
dc.subjectCells, Cultured
dc.subjectChild
dc.subjectCricetinae
dc.subjectCricetulus
dc.subjectFemale
dc.subjectHumans
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectNeural Inhibition
dc.subjectReceptor, Cannabinoid, CB2
dc.subjectSensory Receptor Cells
dc.titleCannabinoid receptor CB2 localisation and agonist-mediated inhibition of capsaicin responses in human sensory neuronsen
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.description.statusPeer reviewed
dcterms.dateAccepted2008
rioxxterms.versionofrecordhttps://doi.org/10.1016/j.pain.2008.06.007
rioxxterms.typeJournal Article/Review
herts.preservation.rarelyaccessedtrue


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