Articles producció científica> Bioquímica i Biotecnologia

Role of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration

  • Datos identificativos

    Identificador: imarina:5131075
    Autores:
    Auladell Cde Lemos LVerdaguer EEttcheto MBusquets OLazarowski ABeas-Zarate COlloquequi JFolch JCamins A
    Resumen:
    Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decades due to their capacity to reproduce with high similarity neuropathological and electroencephalographic features observed in patients with temporal lobe epilepsy (TLE). Kainic acid is one of the most used chemoconvulsants in experimental models. KA administration mainly induces neuronal loss in the hippocampus. We focused the present review inthe c-Jun N-terminal kinase-signaling pathway (JNK), since it has been shown to play a key role in the process of neuronal death following KA activation. Among the three isoforms of JNK (JNK1, JNK2, JNK3), JNK3 is widely localized in the majority of areas of the hippocampus, whereas JNK1 levels are located exclusively in the CA3 and CA4 areas and in dentate gyrus. Disruption of the gene encoding JNK3 in mice renders neuroprotection to KA, since these animals showed a reduction in seizure activity and a diminution in hippocampal neuronal apoptosis. In light of this, JNK3 could be a promising subcellular target for future therapeutic interventions in epilepsy.
  • Otros:

    Autor según el artículo: Auladell C; de Lemos L; Verdaguer E; Ettcheto M; Busquets O; Lazarowski A; Beas-Zarate C; Olloquequi J; Folch J; Camins A
    Departamento: Bioquímica i Biotecnologia
    Autor/es de la URV: Folch Lopez, Jaume
    Palabras clave: Review Neuroprotection Kainic acid Hippocampus Energy metabolism C-jun n-terminal kinase signaling pathway Apoptosis Amyloid beta protein
    Resumen: Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decades due to their capacity to reproduce with high similarity neuropathological and electroencephalographic features observed in patients with temporal lobe epilepsy (TLE). Kainic acid is one of the most used chemoconvulsants in experimental models. KA administration mainly induces neuronal loss in the hippocampus. We focused the present review inthe c-Jun N-terminal kinase-signaling pathway (JNK), since it has been shown to play a key role in the process of neuronal death following KA activation. Among the three isoforms of JNK (JNK1, JNK2, JNK3), JNK3 is widely localized in the majority of areas of the hippocampus, whereas JNK1 levels are located exclusively in the CA3 and CA4 areas and in dentate gyrus. Disruption of the gene encoding JNK3 in mice renders neuroprotection to KA, since these animals showed a reduction in seizure activity and a diminution in hippocampal neuronal apoptosis. In light of this, JNK3 could be a promising subcellular target for future therapeutic interventions in epilepsy.
    Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 10934715
    Direcció de correo del autor: jaume.folch@urv.cat
    Identificador del autor: 0000-0002-5051-8858
    Fecha de alta del registro: 2023-03-05
    Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
    Enlace a la fuente original: https://europepmc.org/article/med/27814647
    Referencia al articulo segun fuente origial: Front Biosci (Landmark Ed). 22 (5): 795-814
    Referencia de l'ítem segons les normes APA: Auladell C; de Lemos L; Verdaguer E; Ettcheto M; Busquets O; Lazarowski A; Beas-Zarate C; Olloquequi J; Folch J; Camins A (2017). Role of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration. Front Biosci (Landmark Ed), 22(5), 795-814. DOI: 10.2741/4517
    URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
    DOI del artículo: 10.2741/4517
    Entidad: Universitat Rovira i Virgili
    Año de publicación de la revista: 2017
    Tipo de publicación: Journal Publications
  • Palabras clave:

    Review
    Neuroprotection
    Kainic acid
    Hippocampus
    Energy metabolism
    C-jun n-terminal kinase signaling pathway
    Apoptosis
    Amyloid beta protein
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