Hippocampal hyperexcitability induced by GABA withdrawal is due to down-regulation of GABAA receptors

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dc.contributor.affiliationInstituto de Fisiología Celular, UNAM, P.O. Box 70-253, Mexico City DF 04510, Mexicoes_ES
dc.contributor.emailjbargas@ifisiol.unam.mxes_ES
dc.creatorCasasola, C.
dc.creatorBargas, J.
dc.creatorArias-Montaño, J.A.
dc.creatorCalixto, E.
dc.creatorMontiel, T.
dc.creatorGalarraga, E.
dc.creatorBrailowsky, S.
dc.creator.identificador"http://orcid.org/0000-0001-9902-9070>Calixto, Eduardoes_ES
dc.date.accessioned2017-06-29T03:52:27Z
dc.date.accessioned2026-03-27T14:33:06Z
dc.date.available2017-06-29T03:52:27Z
dc.date.issued2001es_ES
dc.date.published2001es_ES
dc.description.abstractotrodiomaThe sudden interruption of an intracortical instillation of exogenous  -aminobutyric acid (GABA) generates an epileptic focus in mammals. Seizures elicited by GABA withdrawal (GW) last for weeks. A similar withdrawal-induced hyperexcitability is also produced by several GABAA receptor agonists. This work reports a quantitative analysis of GW-induced hyperexcitability produced in the hippocampus in vitro. GW produced a left-ward displacement of the input/output (I/O) function, suggesting that the postsynaptic component is predominant to explain the hyperexcitability. A decrease in the inhibitory efficacy of the GABAA receptor agonist, muscimol, confirmed that inhibition was impaired. Binding saturation experiments demonstrated a decrease in [3 H]-muscimol binding after GABA withdrawal showing a close correlation with the development of hyperexcitability. All these modifications coursed without changes in receptor affinity (KD) for muscimol or bicuculline as demonstrated by both binding studies and Schild analysis. It is concluded that, in the CA1 region of the hippocampus, it is the number of functional GABAA receptors, and not the affinity of the receptor, what is decreased during GW-induced hyperexcitability.es_ES
dc.description.monthDices_ES
dc.identifier2749es_ES
dc.identifier.citationMercedes Simoni Nieveses_ES
dc.identifier.eissn1872-6844es_ES
dc.identifier.issn0920-1211es_ES
dc.identifier.numero3es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.paginacion257-271es_ES
dc.identifier.placePaíses Bajoses_ES
dc.identifier.urihttps://doi.org/10.1016/S0920-1211(01)00314-Xes_ES
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/4598
dc.identifier.volumen47es_ES
dc.language.isoenges_ES
dc.publisherAmsterdam : Elsevier Science Publisherses_ES
dc.relation47 (3) 257-271 p.es_ES
dc.relationversión del editores_ES
dc.relation.jnabreviadoEPILEPSY RESes_ES
dc.relation.journalEpilepsy Researches_ES
dc.rightsacceso cerradoes_ES
dc.subject.koGABAes_ES
dc.subject.koGABAA receptorses_ES
dc.subject.koEpilepsyes_ES
dc.subject.koGABA withdrawal syndromees_ES
dc.subject.koWithdrawal syndromeses_ES
dc.subject.koHippocampuses_ES
dc.subject.koBenzodiazepine withdrawales_ES
dc.titleHippocampal hyperexcitability induced by GABA withdrawal is due to down-regulation of GABAA receptorses_ES
dc.typeartículoes_ES

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