Transcranial focal electric stimulation avoids P-Glycoprotein over-expression during electrical amygdala kindling and delays epileptogenesis in rats

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dc.contributor.affiliationDepartamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados, Ciudad de México C.P. 14330, Mexico
dc.contributor.emailalevalc@imp.edu.mx (A.V.-C.), lrocha@cinvestav.mx (L.R.)
dc.creatorFonseca-Barriendos, Danieles_ES
dc.creatorCastañeda-Cabral, José Luises_ES
dc.creatorMartínez-Cuevas, Fridaes_ES
dc.creatorBesio, Walteres_ES
dc.creatorValdés-Cruz, Alejandroes_ES
dc.creatorRocha, Luisaes_ES
dc.creator.identificadorhttps://orcid.org/0000-0002-7884-1593 (Fonseca-Barriendos, Daniel)
dc.creator.identificadorhttps://orcid.org/0000-0002-7073-5067 (Castañeda-Cabral, José Luis)
dc.creator.identificadorhttps://orcid.org/0000-0003-2752-5483 (Besio, Walter)
dc.creator.identificadorhttps://orcid.org/0000-0003-0162-7510 (Valdés-Cruz, Alejandro)
dc.creator.identificadorhttps://orcid.org/0000-0003-4495-9427 (Rocha, Luisa)
dc.date2023
dc.date.accessioned2025-04-08T19:09:25Z
dc.date.accessioned2026-03-27T15:31:42Z
dc.date.available2025-04-08T19:09:25Z
dc.date.issued2023
dc.date.published2023
dc.descriptionRecent evidence suggests that P-glycoprotein (P-gp) overexpression mediates hyperexcitability and is associated with epileptogenesis. Transcranial focal electrical stimulation (TFS) delays epileptogenesis and inhibits P-gp overexpression after a generalized seizure. Here, first we measured P-gp expression during epileptogenesis and second, we assessed if TFS antiepileptogenic effect was related with P-gp overexpression avoidance. Male Wistar rats were implanted in right basolateral amygdala and stimulated daily for electrical amygdala kindling (EAK), P-gp expression was assessed during epileptogenesis in relevant brain areas. Stage I group showed 85% increase in P-gp in ipsilateral hippocampus (p < 0.001). Stage III group presented 58% and 57% increase in P-gp in both hippocampi (p < 0.05). Kindled group had 92% and 90% increase in P-gp in both hippocampi (p < 0.01), and 93% and 143% increase in both neocortices (p < 0.01). For the second experiment, TFS was administrated daily after each EAK stimulation for 20 days and P-gp concentration was assessed. No changes were found in the TFS group (p > 0.05). Kindled group showed 132% and 138% increase in P-gp in both hippocampi (p < 0.001) and 51% and 92% increase in both cortices (p < 0.001). Kindled + TFS group presented no changes (p > 0.05). Our experiments revealed that progression of EAK is associated with increased P-gp expression. These changes are structure-specific and dependent on seizure severity. EAK-induced P-gp overexpression would be associated with neuronal hyperexcitability and thus, epileptogenesis. P-gp could be a novel therapeutical target to avoid epileptogenesis. In accordance with this, TFS inhibited P-gp overexpression and interfered with EAK. An important limitation of the present study is that P-gp neuronal expression was not evaluated under the different experimental conditions. Future studies should be carried out to determine P-gp neuronal overexpression in hyperexcitable networks during epileptogenesis. The TFS-induced lessening of P-gp overexpression could be a novel therapeutical strategy to avoid epileptogenesis in high-risk patients.es_ES
dc.formatPDFes_ES
dc.identifierJC28NC23es_ES
dc.identifier.doi10.3390/life13061294
dc.identifier.eissn2075-1729
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.placeSuiza
dc.identifier.urihttps://doi.org/10.3390/life13061294
dc.identifier.urihttps://repositorio.inprf.gob.mx/handle/123456789/8298
dc.language.isoenges_ES
dc.publisherMDPI AGes_ES
dc.relation13(6):1294
dc.relation.jnabreviadoLIFE (BASEL)
dc.relation.journalLife
dc.rightsAcceso Cerradoes_ES
dc.subject.kwP-glycoprotein
dc.subject.kwEpileptogenesis
dc.subject.kwNeuromodulation
dc.subject.kwHippocampus
dc.subject.kwNeocortex
dc.subject.kwKindling
dc.subject.kwTFS
dc.titleTranscranial focal electric stimulation avoids P-Glycoprotein over-expression during electrical amygdala kindling and delays epileptogenesis in ratses_ES
dc.typeArtículoes_ES

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