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Cellular mechanism for specific mechanical antinociception by D2-like receptor at the spinal cord level

dc.creatorAlmanza, Angélicaes_ES
dc.creatorSegura-Chama, Pedroes_ES
dc.creatorLeón-Olea, Marthaes_ES
dc.creatorEnoch, Luises_ES
dc.creatorGarduño-Gutiérrez, Renées_ES
dc.creatorMercado-Reyes, Jonathanes_ES
dc.creatorSimón-Arceo, Karinaes_ES
dc.creatorCoffeen, Uliseses_ES
dc.creatorHernández-Cruz, Arturoes_ES
dc.creatorPellicer, Franciscoes_ES
dc.creatorMercado, Franciscoes_ES
dc.date2019
dc.date.accessioned2022-11-24T20:30:51Z
dc.date.available2022-11-24T20:30:51Z
dc.date.issued2019
dc.identifierJC18NC22es_ES
dc.identifier.issn0306-4522
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7633
dc.identifier.urihttps://doi.org/10.1016/j.neuroscience.2019.08.019
dc.descriptionIntrathecal (i.t.) administration of quinpirole, a dopamine (DA) D2-like receptor agonist, produces antinociception to mechanonociceptive stimuli but not to thermonociceptive stimuli. To determine a cellular mechanism for the specific antinociceptive effect of D2-like receptor activation on mechanonociception, we evaluated the effect of quinpirole on voltage-gated Ca2+ influx in cultured dorsal root ganglion (DRG) neurons and the D2 DA receptor distribution in subpopulations of rat nociceptive DRG neurons. Small-diameter DRG neurons were classified into IB4+ (nonpeptidergic) and IB4- (peptidergic). Intracellular [Ca2+] microfluorometry and voltage-clamp experiments showed that quinpirole reduced Ca2+ influx and inhibited the high voltage-activated Ca2+ current (HVA-ICa) in half of IB4+ neurons, leaving Ca2+ entry and HVA-ICa in IB4- neurons nearly unaffected. Pretreatment with ω-conotoxin MVIIA prevented the effect of quinpirole on HVA-ICa from IB4+ neurons, indicating that quinpirole mainly inhibits CaV2.2 channels. Immunofluorescence experiments showed that D2 DA receptor was present mainly in IB4+ small DRG neurons. Finally, in behavioral experiments in rats, the clinically approved D2-like receptor agonist pramipexole produced spinal antinociception in a similar fashion to quinpirole, with a significant effect only in the mechanonociceptive test. Our results explain, at least in part, why D2-like receptor agonists produce antinociception on mechanonociceptors.es_ES
dc.formatPDFes_ES
dc.language.isoenges_ES
dc.publisherElsevier Sciencees_ES
dc.relation417:81-94
dc.rightsAcceso Cerradoes_ES
dc.titleCellular mechanism for specific mechanical antinociception by D2-like receptor at the spinal cord leveles_ES
dc.typeArtículoes_ES
dc.contributor.affiliationLaboratorio de Fisiología Celular, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Ciudad de México, Mexico
dc.contributor.emailfmercado@imp.edu.mx (F. Mercado)
dc.relation.jnabreviadoNEUROSCIENCE
dc.relation.journalNeuroscience
dc.identifier.placeEstados Unidos
dc.date.published2019
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.eissn1873-7544
dc.identifier.doi10.1016/j.neuroscience.2019.08.019
dc.subject.kwDopamine
dc.subject.kwD2-like receptors
dc.subject.kwMechanonociception
dc.subject.kwCaV2.2 channels
dc.subject.kwNeurotransmitter release
dc.subject.kwAntinociception


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