dc.creatorOliveira, MCG
dc.creatorPelegrini-Da-Silva, A
dc.creatorParada, CA
dc.creatorTambeli, CH
dc.date2007
dc.date42430
dc.date2014-11-16T10:10:56Z
dc.date2015-11-26T17:24:26Z
dc.date2014-11-16T10:10:56Z
dc.date2015-11-26T17:24:26Z
dc.date.accessioned2018-03-29T00:11:44Z
dc.date.available2018-03-29T00:11:44Z
dc.identifierNeuroscience. Pergamon-elsevier Science Ltd, v. 145, n. 2, n. 708, n. 714, 2007.
dc.identifier0306-4522
dc.identifierWOS:000245045800029
dc.identifier10.1016/j.neuroscience.2006.12.021
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/52677
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/52677
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/52677
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1284079
dc.descriptionWe have recently demonstrated that s.c.-injected 5-hydroxytryptamine (5-HT) induces nociception by an indirect action on the primary afferent nociceptor in addition to its previously described direct action. Although the mechanisms mediating hyperalgesia can be quite separate and distinct from those mediating nociception, the aim of this study was to test the hypothesis that 5-HT induces mechanical hyperalgesia by mechanisms similar to those mediating nociception. s.c. injection of 5-HT induced a dose-dependent mechanical hyperalgesia measured by the mechanical paw withdrawal nociceptive threshold test in the rat. 5-HT-induced hyperalgesia was significantly reduced by local blockade of the 5-HT3 receptor by tropisetron, by the nonspecific selectin inhibitor fucoidan, by the cyclooxygenase inhibitor indomethacin, by guanethidine depletion of norepinephrine in the sympathetic terminals, and by local blockade of the beta(1)- or beta(2)-adrenergic receptor by atenolol or ICI 118,551, respectively. Taken together, these findings indicate that like nociception, hyperalgesia induced by the injection of 5-HT in the s.c. tissue is also mediated by an indirect action of 5-HT on the primary afferent nociceptor. This indirect hyperalgesic action of 5-HT is mediated by a combination of mechanisms involved in inflammation such as neutrophil migration and the local release of prostaglandin and norepinephrine. However, in contrast to nociception, hyperalgesia induced by 5-HT in the s.c. tissue is mediated by a norepinephrine-dependent mechanism that involves the activation of peripheral beta(2) adrenoceptors. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.
dc.description145
dc.description2
dc.description708
dc.description714
dc.languageen
dc.publisherPergamon-elsevier Science Ltd
dc.publisherOxford
dc.publisherInglaterra
dc.relationNeuroscience
dc.relationNeuroscience
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectserotonin
dc.subjecthyperalgesia
dc.subjectprostaglandins
dc.subjectnorepinephrine
dc.subjectneutrophil migration
dc.subjects.c. tissue
dc.subjectProtein-kinase
dc.subjectPlasma Extravasation
dc.subjectThermal Hyperalgesia
dc.subjectRat
dc.subjectSerotonin
dc.subjectPain
dc.subjectReceptors
dc.subject5-hydroxytryptamine
dc.subjectActivation
dc.subjectTerminals
dc.title5-HT acts on nociceptive primary afferents through an indirect mechanism to induce hyperalgesia in the subcutaneous tissue
dc.typeArtículos de revistas


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