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Transcranial focal electric stimulation avoids P-Glycoprotein over-expression during electrical amygdala kindling and delays epileptogenesis in rats
dc.creator | Fonseca-Barriendos, Daniel | es_ES |
dc.creator | Castañeda-Cabral, José Luis | es_ES |
dc.creator | Martínez-Cuevas, Frida | es_ES |
dc.creator | Besio, Walter | es_ES |
dc.creator | Valdés-Cruz, Alejandro | es_ES |
dc.creator | Rocha, Luisa | es_ES |
dc.date | 2023 | |
dc.date.accessioned | 2025-04-08T19:09:25Z | |
dc.date.available | 2025-04-08T19:09:25Z | |
dc.date.issued | 2023 | |
dc.identifier | JC28NC23 | es_ES |
dc.identifier.uri | http://repositorio.inprf.gob.mx/handle/123456789/8298 | |
dc.identifier.uri | https://doi.org/10.3390/life13061294 | |
dc.description | Recent 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.format | es_ES | |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI AG | es_ES |
dc.relation | 13(6):1294 | |
dc.rights | Acceso Cerrado | es_ES |
dc.title | Transcranial focal electric stimulation avoids P-Glycoprotein over-expression during electrical amygdala kindling and delays epileptogenesis in rats | es_ES |
dc.type | Artículo | es_ES |
dc.contributor.affiliation | Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados, Ciudad de México C.P. 14330, Mexico | |
dc.contributor.email | alevalc@imp.edu.mx (A.V.-C.), lrocha@cinvestav.mx (L.R.) | |
dc.relation.jnabreviado | LIFE (BASEL) | |
dc.relation.journal | Life | |
dc.identifier.place | Suiza | |
dc.date.published | 2023 | |
dc.identifier.organizacion | Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz | |
dc.identifier.eissn | 2075-1729 | |
dc.identifier.doi | 10.3390/life13061294 | |
dc.subject.kw | P-glycoprotein | |
dc.subject.kw | Epileptogenesis | |
dc.subject.kw | Neuromodulation | |
dc.subject.kw | Hippocampus | |
dc.subject.kw | Neocortex | |
dc.subject.kw | Kindling | |
dc.subject.kw | TFS |
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