Articles producció científica> Bioquímica i Biotecnologia

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

  • Identification data

    Identifier: imarina:5131075
    Authors:
    Auladell Cde Lemos LVerdaguer EEttcheto MBusquets OLazarowski ABeas-Zarate COlloquequi JFolch JCamins A
    Abstract:
    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.
  • Others:

    Author, as appears in the article.: Auladell C; de Lemos L; Verdaguer E; Ettcheto M; Busquets O; Lazarowski A; Beas-Zarate C; Olloquequi J; Folch J; Camins A
    Department: Bioquímica i Biotecnologia
    URV's Author/s: Folch Lopez, Jaume
    Keywords: Review Neuroprotection Kainic acid Hippocampus Energy metabolism C-jun n-terminal kinase signaling pathway Apoptosis Amyloid beta protein
    Abstract: 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.
    licence for use: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 10934715
    Author's mail: jaume.folch@urv.cat
    Author identifier: 0000-0002-5051-8858
    Record's date: 2023-03-05
    Papper version: info:eu-repo/semantics/publishedVersion
    Link to the original source: https://europepmc.org/article/med/27814647
    Papper original source: Front Biosci (Landmark Ed). 22 (5): 795-814
    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
    Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
    Article's DOI: 10.2741/4517
    Entity: Universitat Rovira i Virgili
    Journal publication year: 2017
    Publication Type: Journal Publications
  • Keywords:

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