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dc.creatorOrtiz , G.G.
dc.creatorSánchez-Ruiz, Y.
dc.creatorTan, D.X.
dc.creatorReiter, R.J.
dc.creatorBenítez-King, G.
dc.creatorBeas-Zárate, C.
dc.date.accessioned2017-06-29T04:25:52Z
dc.date.available2017-06-29T04:25:52Z
dc.date.issued2001es_ES
dc.identifier337es_ES
dc.identifier.issn0742-3098es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/5029
dc.identifier.urihttps://doi.org/10.1034/j.1600-079X.2001.310109.xes_ES
dc.language.isoenges_ES
dc.relation31 (1) 62-67 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshAntioxidants-Pharmacologyes_ES
dc.subject.meshEstradiol-Analogs & derivativeses_ES
dc.subject.meshPharmacologyes_ES
dc.subject.meshFree Radical Scavengers-Pharmacologyes_ES
dc.subject.meshHippocampus-Drug effectses_ES
dc.subject.meshInjurieses_ES
dc.subject.meshSecretiones_ES
dc.subject.meshKainic Acid-Antagonists & inhibitors-Toxicityes_ES
dc.subject.meshMalees_ES
dc.subject.meshMelatonines_ES
dc.titleMelatonin, vitamin E, and estrogen reduce damage induced by kainic acid in the hippocampus: potassium-stimulated GABA releasees_ES
dc.typearticlees_ES
dc.contributor.affiliationDivisión de Neurociencias, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Méxicoes_ES
dc.contributor.emailgenarogabriel@yahoo.comes_ES
dc.relation.jnabreviadoJ PINEAL RESes_ES
dc.relation.journalJournal of pineal researches_ES
dc.date.published2001es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.description.monthAgoes_ES
dc.description.abstractotrodiomaMelatonin, vitamin E and estrogen have been shown to exert neuroprotective effects against kainic acid (KA)-induced damage in the hippocampus. The aim of the present study was to examine the changes in potassium-evoked gamma-aminobutyric acid (GABA) release in the hippocampus of KA-treated rats and to test the possible protective effects of melatonin, vitamin E or estrogen. Following the treatment of mice with KA, a marked reduction in potassium-evoked [3H]GABA release was observed. Melatonin or estrogen prevented the reduction in potassium-evoked GABA release due to kainate administration. Vitamin E also exhibited some protective effect, but it was less than that provided by melatonin or estrogen. Melatonin, estrogen and, to a lesser extent, vitamin E reduce the physiological toxicity of KA. Since KA is believed to cause neuronal alterations via oxidative processes, it is assumed that the free radical scavenging and oxidative properties of melatonin, estrogen and vitamin E account for the protective.es_ES
dc.subject.meshmPharmacologyes_ES
dc.subject.meshmFree Radical Scavengers-Pharmacologyes_ES
dc.subject.meshmHippocampus-Drug effectses_ES
dc.subject.meshmHippocampus-Injurieses_ES
dc.subject.meshmHippocampus-Secretiones_ES
dc.subject.meshmKainic acid-Antagonists & inhibitorses_ES
dc.subject.meshmKainic acid-Toxicityes_ES
dc.subject.meshmMalees_ES
dc.subject.meshmMelatonines_ES
dc.subject.kwAnimaleses_ES
dc.subject.kwAntioxidantes-Farmacologíaes_ES
dc.subject.kwEstradiol-Análogos y derivadoses_ES
dc.subject.kwFarmacologyes_ES


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