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dc.creatorCasasola, C.
dc.creatorMontiel, T.
dc.creatorCalixto, E.
dc.creatorBrailowskyb, S.
dc.date.accessioned2017-06-29T03:52:57Z
dc.date.available2017-06-29T03:52:57Z
dc.date.issued2004es_ES
dc.identifier2755es_ES
dc.identifier.issn0306-4522es_ES
dc.identifier.urihttps://doi.org/10.1016/j.neuroscience.2004.03.029es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4604
dc.description.abstractes_ES
dc.language.isoenges_ES
dc.publisher[New York?] : Elsevier Sciencees_ES
dc.relation126 (1) 163-171 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshBicuculline/pharmacologyes_ES
dc.subject.meshElectroencephalographyes_ES
dc.subject.meshGABA Antagonists/pharmacologyes_ES
dc.subject.meshGABA-A Receptor Antagonistses_ES
dc.subject.meshHippocampus/drug effectses_ES
dc.subject.meshHippocampus/physiologyes_ES
dc.subject.meshLong-Term Potentiation/drug effectses_ES
dc.subject.meshLong-Term Potentiation/physiologyes_ES
dc.subject.meshMalees_ES
dc.subject.meshNeuronal Plasticity/drug effectses_ES
dc.subject.meshNeuronal Plasticity/physiologyes_ES
dc.subject.meshRatses_ES
dc.subject.meshRats, Wistares_ES
dc.subject.meshReceptors, GABA-A/physiologyes_ES
dc.subject.meshSynaptic Transmission/physiologyes_ES
dc.subject.meshgamma-Aminobutyric Acid/physiologyes_ES
dc.titleHyperexcitability induced by gaba withdrawal facilitates hippocampal long-term potentiationes_ES
dc.title.alternativees_ES
dc.typeartículoes_ES
dc.contributor.affiliationDepto. de Psicofisiología, Facultad de Psicología, Universidad Nacional Autónoma de México. Av. Universidad 3004, Col. Copilco Universidad, C.P. 04510, Mexicoes_ES
dc.contributor.emailcasasola@ifc.unam.mxes_ES
dc.relation.jnabreviadoNEUROSCIENCEes_ES
dc.relation.journalNeurosciencees_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2004es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1873-7544es_ES
dc.identifier.doi10.1016/j.neuroscience.2004.03.029es_ES
dc.description.monthes_ES
dc.description.abstractotrodiomaAbstract—In some mammals, epileptic seizures have been induced in the cerebral cortex, hippocampus and other limbic structures after the sudden suppression of chronically infused GABA. This hyperexcitability state induced by the endogenous neurotransmitter resembles the withdrawal seizure-responses to other GABAA receptor agonists such as benzodiazepines, barbiturates and alcohol. Hyperexcitability induced by GABA withdrawal also persists in in vitro preparation. Hippocampal slices, obtained from rats with seizures induced by GABA-withdrawal showed field potential oscillations and paroxysmal activity in the Ammon’s horn region 1. During GABA-withdrawal hyperexcitability the threshold of hippocampal long-term potentiation (LTP) decreased to a point in which a brief frequency stimulation that normally failed to produce long lasting changes in synaptic strength, was now able to induce LTP. Facilitation of the LTP induction was associated with a decreased GABAAmediated inhibitory activity, because the effect of the GABAA receptor antagonist, bicuculline, was occluded during hyperexcitability and the dose-response curve for bicuculline showed a 50% efficacy reduction with a shift in the effective concentration required for half-maximal activation from 4.5– 1.1  M relative to controls. Nevertheless, the dissociation constant of the antagonist did not change significantly. Our results support the idea that changes in hippocampal plasticity under altered inhibitory neurotransmission states, like those induced by withdrawal syndromes to anxiolytic, sedative or anticonvulsant drugs may be engaged during seizures.es_ES
dc.subject.meshmes_ES
dc.subject.kwes_ES
dc.subject.koLTPes_ES
dc.subject.koGABA Withdrawales_ES
dc.subject.koPlasticityes_ES
dc.subject.koEpilepsyes_ES
dc.subject.koHippocampuses_ES
dc.subject.koGABAA Receptores_ES


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