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Modulation of voltage-gated Ca2+ current in vestibular hair cells by nitric oxide

dc.creatorAlmanza, Angélica
dc.creatorNavarrete, Francisco
dc.creatorVega, Rosario
dc.creatorSoto, Enrique
dc.date.accessioned2017-06-29T04:00:07Z
dc.date.available2017-06-29T04:00:07Z
dc.date.issued2007es_ES
dc.identifier2834es_ES
dc.identifier.issn0022-3077es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4683
dc.identifier.urihttps://doi.org/10.1152/jn.00849.2006es_ES
dc.description.abstractes_ES
dc.language.isoenges_ES
dc.publisherBethesda Md : American Physiological Societyes_ES
dc.relation97 (2) 1188-1195 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshCalcium Channels, L-Type/drug effectses_ES
dc.subject.meshCalcium Channels, L-Type/physiologyes_ES
dc.subject.meshCarbazoles/pharmacologyes_ES
dc.subject.meshCell Separationes_ES
dc.subject.meshCyclic GMP/analogs & derivativeses_ES
dc.subject.meshCyclic GMP/pharmacologyes_ES
dc.subject.meshCyclic GMP/physiologyes_ES
dc.subject.meshData Interpretation, Statisticales_ES
dc.subject.meshEnzyme Inhibitors/pharmacologyes_ES
dc.subject.meshEthylmaleimide/pharmacologyes_ES
dc.subject.meshFree Radical Scavengers/pharmacologyes_ES
dc.subject.meshHair Cells, Vestibular/drug effectses_ES
dc.subject.meshHair Cells, Vestibular/physiologyes_ES
dc.subject.meshIn Vitro Techniqueses_ES
dc.subject.meshIndoles/pharmacologyes_ES
dc.subject.meshMolsidomine/analogs & derivativeses_ES
dc.subject.meshMolsidomine/pharmacologyes_ES
dc.subject.meshNitric Oxide/pharmacologyes_ES
dc.subject.meshNitric Oxide/physiologyes_ES
dc.subject.meshNitroprusside/pharmacologyes_ES
dc.subject.meshPatch-Clamp Techniqueses_ES
dc.subject.meshRatses_ES
dc.subject.meshRats, Long-Evanses_ES
dc.subject.meshSignal Transduction/physiologyes_ES
dc.titleModulation of voltage-gated Ca2+ current in vestibular hair cells by nitric oxidees_ES
dc.title.alternativees_ES
dc.typeartículoes_ES
dc.contributor.affiliationInstituto de Fisiología, Universidad Autónoma de Puebla, Puebla, Mexicoes_ES
dc.contributor.emailesoto@siu.buap.mxes_ES
dc.relation.jnabreviadoJ NEUROPHYSIOLes_ES
dc.relation.journalJournal of Neurophysiologyes_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2007es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1522-1598es_ES
dc.identifier.doi10.1152/jn.00849.2006es_ES
dc.description.monthFebes_ES
dc.description.abstractotrodiomaThe structural elements of the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) signaling pathway have been described in the vestibular peripheral system. However, the functions of NO in the vestibular endorgans are still not clear. We evaluated the action of NO on the Ca(2+) currents in hair cells isolated from the semicircular canal crista ampullaris of the rat (P14-P18) by using the whole cell and perforated-cell patch-clamp technique. The NO donors 3-morpholinosydnonimine (SIN-1), sodium nitroprusside (SNP), and (+/-)-(E)-4-ethyl-2-[(Z)-hydroxyimino]-5-nitro-3-hexen-1-yl-nicotinamide (NOR-4) inhibited the Ca(2+) current in hair cells in a voltage-independent manner. The NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO) prevented the inhibitory effect of SNP on the Ca(2+) current. The selective inhibitor of the soluble form of the enzyme guanylate cyclase (sGC), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), also decreased the SNP-induced inhibition of the Ca(2+) current. The membrane-permeant cGMP analogue 8-Br-cGMP mimicked the SNP effect. KT-5823, a specific inhibitor of cGMP-dependent protein kinase (PGK), prevented the inhibition of the Ca(2+) current by SNP and 8-Br-cGMP. In the presence of N-ethylmaleimide (NEM), a sulfhydryl alkylating agent that prevents the S-nitrosylation reaction, the SNP effect on the Ca(2+) current was significantly diminished. These results demonstrated that NO inhibits in a voltage-independent manner the voltage-activated Ca(2+) current in rat vestibular hair cells by the activation of a cGMP-signaling pathway and through a direct action on the channel protein by a S-nitrosylation reaction. The inhibition of the Ca(2+) current by NO may contribute to the regulation of the intracellular Ca(2+) concentration and hair-cell synaptic transmission.es_ES
dc.subject.meshmes_ES
dc.subject.kwes_ES
dc.subject.koes_ES


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