Peripheral sympathetic component of the temporomandibular joint inflammatory pain in rats

dc.creatorRodrigues, LLFR
dc.creatorOliveira, MCG
dc.creatorPelegrini-Da-Silva, A
dc.creatorVelga, MCFD
dc.creatorParada, CA
dc.creatorTambeli, CH
dc.date2006
dc.dateDEC
dc.date2014-11-16T02:21:24Z
dc.date2015-11-26T16:31:23Z
dc.date2014-11-16T02:21:24Z
dc.date2015-11-26T16:31:23Z
dc.date.accessioned2018-03-28T23:12:24Z
dc.date.available2018-03-28T23:12:24Z
dc.identifierJournal Of Pain. Churchill Livingstone, v. 7, n. 12, n. 929, n. 936, 2006.
dc.identifier1526-5900
dc.identifierWOS:000243188100008
dc.identifier10.1016/j.jpain.2006.05.006
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/59340
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/59340
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/59340
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1270189
dc.descriptionThe aim of this study was to further validate our carrageenan-induced temporomanclibular joint (TMJ) inflammatory hyperalgesia model in rats by showing that administration of indomethacin before the initiation of inflammation would diminish the TMJ hyperalgesia. Using this model, we investigated whether norepinephrine and local beta-adrenoceptors contribute to the development of inflammatory TMJ hyperalgesia. Carrageenan-induced TMJ hyperalgesia was assessed by measuring the behavioral nociceptive responses, such as rubbing the orofacial region and flinching the head, induced by the injection of a low dose of 5-hydroxytryptamine into the TMJ sensitized 1 h before by a TMJ injection of carrageenan. Blockade of prostaglandin synthesis by indomethacin prior to initiation of inflammation by carrageenan significantly attenuated the TMJ hyperalgesia. The guanethidine depletion of norepinephrine or the blockade of P, but not the blockade of the beta(1)-adrenoceptor by the selective adrenoceptor antagonists ICI 118.55 and atenolol, respectively, significantly reduced carrageenan-induced TMJ hyperalgesia. in the present study, we further validated our carrageenan-induced TMJ hyperalgesia model to study the mechanisms involved in inflammatory TMJ hyperalgesia and to test the analgesic effect of different types of peripheral analgesics. We also demonstrated that norepinephrine released at the site of injury contributes to the development of the inflammatory TMJ hyperalgesia by the activation of beta(2)-adrenoceptors. Perspective: The findings that local sympathomimetic amines contribute to the inflammatory TMJ hyperalgesia by activating beta(2)-adrenoceptors may be relevant to clinical TMJ inflammatory pain states less sensitive to nonsteroidal anti-inflammatory drugs. (c) 2006 by the American Pain Society.
dc.description7
dc.description12
dc.description929
dc.description936
dc.languageen
dc.publisherChurchill Livingstone
dc.publisherEdinburgh
dc.publisherEscócia
dc.relationJournal Of Pain
dc.relationJ. Pain
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectTMJ
dc.subjectcarrageenan
dc.subjectchemical hyperalgesia
dc.subjectsympathomimetic amines
dc.subjectbeta-adrenoceptors
dc.subjectBrain-stem Mechanisms
dc.subjectIrritant Application
dc.subjectReceptor Mechanisms
dc.subjectSynovial-fluid
dc.subjectDorsal-horn
dc.subjectSpinal-cord
dc.subjectTmj Pain
dc.subjectDisorders
dc.subjectHyperalgesia
dc.subjectNeurons
dc.titlePeripheral sympathetic component of the temporomandibular joint inflammatory pain in rats
dc.typeArtículos de revistas


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