dc.contributorUreña-Guerrero, M.E., Departamento de Biología Celular y Molecular, Centro Universitario de Ciencias Biológicas y Agropecuarias, Universidad de Guadalajara, Km. 15.5 Carretera-Guadalajara-Nogales, Predio Las Agujas, Zapopan, Jalisco, Mexico; Feria-Velasco, A.I., Departamento de Biología Celular y Molecular, Centro Universitario de Ciencias Biológicas y Agropecuarias, Universidad de Guadalajara, Km. 15.5 Carretera-Guadalajara-Nogales, Predio Las Agujas, Zapopan, Jalisco, Mexico; Gudiño-Cabrera, G., Departamento de Biología Celular y Molecular, Centro Universitario de Ciencias Biológicas y Agropecuarias, Universidad de Guadalajara, Km. 15.5 Carretera-Guadalajara-Nogales, Predio Las Agujas, Zapopan, Jalisco, Mexico; Espuny, A.C., Department of Pharmacology and Biomedical Chemistry, University of Barcelona, Avenida Diagonal 643, Barcelona, Spain; Beas-Zárate, C., Departamento de Biología Celular y Molecular, Centro Universitario de Ciencias Biológicas y Agropecuarias, Universidad de Guadalajara, Km. 15.5 Carretera-Guadalajara-Nogales, Predio Las Agujas, Zapopan, Jalisco, Mexico
dc.contributorBeas-Zárate, Carlos., Universidad de Guadalajara. Centro Universitario de Ciencias Biológicas y Agropecuarias
dc.creatorUrena-Guerrero M.E
dc.creatorFeria-Velasco A.I
dc.creatorGudino-Cabrera G
dc.creatorEspuny A.C
dc.creatorBeas-Zárate, Carlos
dc.date.accessioned2015-09-15T19:20:16Z
dc.date.accessioned2022-11-02T15:29:54Z
dc.date.available2015-09-15T19:20:16Z
dc.date.available2022-11-02T15:29:54Z
dc.date.created2015-09-15T19:20:16Z
dc.date.issued2013
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84929571155&partnerID=40&md5=ab194ab9f85a70467c91429351cfa7c8
dc.identifierhttp://hdl.handle.net/20.500.12104/45795
dc.identifier10.1007/978-1-4614-6464-8_5
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/5014719
dc.description.abstractThe neuronal damage and seizures are two processes closely related not only as cause and effect in reciprocal way but also through the cellular mechanisms and signaling pathways that they share. Therefore, increments in extracellular levels of the glutamate excitatory neurotransmitter, the over-activation of its receptors and the excessive neuronal excitation, have been described as events associated to both processes. In general, if neurons are not able to recover from its excessive excitation, then they die by excitotoxicity. Our group has showed that the excitotoxicity induced by monosodium glutamate in early developmental stages is able to produce significant modifications in glutamatergic and GABAergic neurotransmission systems. Moreover, preliminary results indicate that those modifications are able to increase the seizure susceptibility in the adulthood, particularly when the convulsive drug 4-aminopyridine and the GABA antagonists are employed to induce the seizures, but not when NMDA agonists are used. Through this chapter the topics mentioned above and the hypothesis about the excitotoxic neonatal damage is able to induce a kind of pharmacoresistance to NMDA analogs will be discussed with in detail. © 2013 Springer Science+Business Media, LLC. All rights are reserved.
dc.relationScopus
dc.relationPharmacoresistance in Epilepsy: From Genes and Molecules to Promising Therapies
dc.relation59
dc.relation76
dc.titleModifications in the seizures susceptibility by excitotoxic neuronal damage and its possible relationship with the pharmacoresistance
dc.typeBook Chapter


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