dc.creator | Tambeli, C H | |
dc.creator | Oliveira, M C G | |
dc.creator | Clemente, J T | |
dc.creator | Pelegrini-da-Silva, A | |
dc.creator | Parada, C A | |
dc.date | 2006-Sep | |
dc.date | 2015-11-27T13:05:30Z | |
dc.date | 2015-11-27T13:05:30Z | |
dc.date.accessioned | 2018-03-29T01:02:54Z | |
dc.date.available | 2018-03-29T01:02:54Z | |
dc.identifier | Neuroscience. v. 141, n. 3, p. 1517-24, 2006-Sep. | |
dc.identifier | 0306-4522 | |
dc.identifier | 10.1016/j.neuroscience.2006.04.030 | |
dc.identifier | http://www.ncbi.nlm.nih.gov/pubmed/16750893 | |
dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/196796 | |
dc.identifier | 16750893 | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1297029 | |
dc.description | The 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.description | 141 | |
dc.description | 1517-24 | |
dc.language | eng | |
dc.relation | Neuroscience | |
dc.relation | Neuroscience | |
dc.rights | fechado | |
dc.rights | | |
dc.source | PubMed | |
dc.subject | Adrenergic Beta-antagonists | |
dc.subject | Afferent Pathways | |
dc.subject | Analysis Of Variance | |
dc.subject | Animals | |
dc.subject | Anti-inflammatory Agents, Non-steroidal | |
dc.subject | Anticoagulants | |
dc.subject | Atenolol | |
dc.subject | Behavior, Animal | |
dc.subject | Benzazepines | |
dc.subject | Dopamine Antagonists | |
dc.subject | Dose-response Relationship, Drug | |
dc.subject | Drug Interactions | |
dc.subject | Indomethacin | |
dc.subject | Male | |
dc.subject | Neutrophils | |
dc.subject | Nociceptors | |
dc.subject | Pain | |
dc.subject | Pain Measurement | |
dc.subject | Polysaccharides | |
dc.subject | Propanolamines | |
dc.subject | Rats | |
dc.subject | Rats, Wistar | |
dc.subject | Serotonin | |
dc.subject | Serotonin Agents | |
dc.subject | Time Factors | |
dc.title | A Novel Mechanism Involved In 5-hydroxytryptamine-induced Nociception: The Indirect Activation Of Primary Afferents. | |
dc.type | Artículos de revistas | |