A Novel Mechanism Involved In 5-hydroxytryptamine-induced Nociception: The Indirect Activation Of Primary Afferents.

dc.creatorTambeli, C H
dc.creatorOliveira, M C G
dc.creatorClemente, J T
dc.creatorPelegrini-da-Silva, A
dc.creatorParada, C A
dc.date2006-Sep
dc.date2015-11-27T13:05:30Z
dc.date2015-11-27T13:05:30Z
dc.date.accessioned2018-03-29T01:02:54Z
dc.date.available2018-03-29T01:02:54Z
dc.identifierNeuroscience. v. 141, n. 3, p. 1517-24, 2006-Sep.
dc.identifier0306-4522
dc.identifier10.1016/j.neuroscience.2006.04.030
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/16750893
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/196796
dc.identifier16750893
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1297029
dc.descriptionThe aim of this study was to test the hypothesis that 5-hydroxytryptamine induces nociception by an indirect action on the primary afferent nociceptor in addition to its previously described direct action. Injection of 5-hydroxytryptamine into the s.c. tissue of the hind paw of rats produced nociceptive flinch behavior and inflammatory cell migration, that were significantly reduced by the nonspecific selectin inhibitor fucoidan. 5-Hydroxytryptamine-induced nociception was also significantly reduced by local blockade of the 5-HT3 receptor by tropisetron, by the cyclooxygenase inhibitor indomethacin and by local blockade of the beta1-adrenergic receptor or of the D1 receptor by atenolol or SCH 23390, respectively. Neither guanethidine depletion of norepinephrine in the sympathetic terminals nor local blockade of the beta2-adrenergic receptor by ICI-118,551 significantly reduced 5-hydroxytryptamine-induced nociception. Taken together, these findings indicate that 5-hydroxytryptamine induces nociception by a novel, indirect and norepinephrine-independent mechanism mediated by neutrophil migration and local release of prostaglandin and dopamine. Furthermore, to test whether dopamine acts on beta1-adrenergic and/or D1 receptor to contribute to 5-hydroxytryptamine-induced nociception, dopamine was s.c. injected either alone or combined with atenolol or with SCH 23390. S.c.-injected dopamine also produced a dose-dependent nociceptive behavior that was significantly reduced by both SCH 23390 and atenolol. Based on that it is proposed that dopamine, once released, activates D1 and beta1-adrenergic receptors to contribute to 5-hydroxytryptamine-induced nociception.
dc.description141
dc.description1517-24
dc.languageeng
dc.relationNeuroscience
dc.relationNeuroscience
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAdrenergic Beta-antagonists
dc.subjectAfferent Pathways
dc.subjectAnalysis Of Variance
dc.subjectAnimals
dc.subjectAnti-inflammatory Agents, Non-steroidal
dc.subjectAnticoagulants
dc.subjectAtenolol
dc.subjectBehavior, Animal
dc.subjectBenzazepines
dc.subjectDopamine Antagonists
dc.subjectDose-response Relationship, Drug
dc.subjectDrug Interactions
dc.subjectIndomethacin
dc.subjectMale
dc.subjectNeutrophils
dc.subjectNociceptors
dc.subjectPain
dc.subjectPain Measurement
dc.subjectPolysaccharides
dc.subjectPropanolamines
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectSerotonin
dc.subjectSerotonin Agents
dc.subjectTime Factors
dc.titleA Novel Mechanism Involved In 5-hydroxytryptamine-induced Nociception: The Indirect Activation Of Primary Afferents.
dc.typeArtículos de revistas


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