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Inflammatory nociception diminishes dopamine release and increases dopamine D2 receptor mRNA in the rat's insular cortex

dc.creatorCoffeen, Ulises
dc.creatorOrtega-Legaspi, J. Manuel
dc.creatorGortari, Patricia de
dc.creatorSimón-Arceo, Karina
dc.creatorJaimes, Orlando
dc.creatorAmaya, María Isabel
dc.creatorPellicer, Francisco
dc.date.accessioned2017-06-30T01:38:53Z
dc.date.available2017-06-30T01:38:53Z
dc.date.issued2010es_ES
dc.identifier1501es_ES
dc.identifier.issn1744-8069es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6181
dc.identifier.urihttps://doi.org/10.1186/1744-8069-6-75es_ES
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994804/es_ES
dc.language.isoenges_ES
dc.relation6 (75) 1-8 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleInflammatory nociception diminishes dopamine release and increases dopamine D2 receptor mRNA in the rat's insular cortexes_ES
dc.typearticlees_ES
dc.contributor.affiliationLaboratorio de Neurofisiología Integrativa, Dirección de Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente, Méxicoes_ES
dc.contributor.emailpellicer@imp.edu.mxes_ES
dc.relation.jnabreviadoMOL PAINes_ES
dc.relation.journalMolecular Paines_ES
dc.identifier.placeInglaterraes_ES
dc.date.published2010es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1744-8069es_ES
dc.identifier.doi10.1186/1744-8069-6-75es_ES
dc.description.monthNoves_ES
dc.description.abstractotrodiomaThe insular cortex (IC) receives somatosensory afferent input and has been related to nociceptive input. It has dopaminergic terminals and D1 (D1R) -excitatory- and D2 (D2R) -inhibitory- receptors. D2R activation with a selective agonist, as well as D1R blockade with antagonists in the IC, diminish neuropathic nociception in a nerve transection model. An intraplantar injection of carrageenan and acute thermonociception (plantar test) were performed to measure the response to inflammation (paw withdrawal latency, PWL). Simultaneously, a freely moving microdyalisis technique and HPLC were used to measure the release of dopamine and its metabolites in the IC. Plantar test was applied prior, one and three hours after inflammation. Also, mRNA levels of D1 and D2R's were measured in the IC after three hours of inflammation. RESULTS: The results showed a gradual decrease in the release of dopamine, Dopac and HVA after inflammation. The decrease correlates with a decrease in PWL. D2R's increased their mRNA expression compared to the controls. In regard of D1R's, there was a decrease in their mRNA levels compared to the controls. CONCLUSIONS: Our results showed that the decreased extracellular levels of dopamine induced by inflammation correlated with the level of pain-related behaviour. These results also showed the increase in dopaminergic mediated inhibition by an increase in D2R's and a decrease in D1R's mRNA. There is a possible differential mechanism regarding the regulation of excitatory and inhibitory dopaminergic receptors triggered by inflammationes_ES
dc.subject.koAnimalses_ES
dc.subject.koCerebral Cortexes_ES
dc.subject.koDopaminees_ES
dc.subject.koanalysises_ES
dc.subject.koDopaminees_ES
dc.subject.kometabolismes_ES
dc.subject.koGene Expression Regulationes_ES
dc.subject.koInflammationes_ES
dc.subject.kometabolismes_ES
dc.subject.koNociceptorses_ES
dc.subject.kometabolismes_ES
dc.subject.koPain*es_ES
dc.subject.kogeneticses_ES
dc.subject.koPain*es_ES
dc.subject.kometabolismes_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.kogeneticses_ES
dc.subject.koRatses_ES
dc.subject.koReceptors, Dopamine D1es_ES
dc.subject.kogeneticses_ES
dc.subject.koReceptors, Dopamine D2es_ES
dc.subject.kogeneticses_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.koReceptors, Dopamine D1es_ES
dc.subject.koReceptors, Dopamine D2es_ES


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