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

dc.contributor.authorAuladell C.
dc.contributor.authorDe Lemos L.
dc.contributor.authorVerdaguer E.
dc.contributor.authorEttcheto M.
dc.contributor.authorBusquets O.
dc.contributor.authorLazarowski A.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorOlloquequi J.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:12:32Z
dc.date.available2020-09-02T22:12:32Z
dc.date.issued2017
dc.identifier10.2741/4517
dc.identifier.citation22, 5, 795-814
dc.identifier.issn10939946
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3646
dc.descriptionChemoconvulsants 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.
dc.language.isoen
dc.publisherFrontiers in Bioscience
dc.subjectApoptosis
dc.subjectC-Jun N-terminal kinase signaling pathway
dc.subjectHippocampuS
dc.subjectKainic acid
dc.subjectNeuroprotection
dc.subjectReview
dc.subjectanticonvulsive agent
dc.subjectisoenzyme
dc.subjectkainic acid
dc.subjectmitogen activated protein kinase 10
dc.subjectsignal transducing adaptor protein
dc.subjectstress activated protein kinase
dc.subjectanimal
dc.subjectchemically induced
dc.subjectdeficiency
dc.subjectdisease model
dc.subjectdrug effects
dc.subjectenzymology
dc.subjectepilepsy
dc.subjectgenetics
dc.subjecthippocampus
dc.subjecthuman
dc.subjectknockout mouse
dc.subjectMAPK signaling
dc.subjectmetabolism
dc.subjectmouse
dc.subjectnerve degeneration
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectAdaptor Proteins, Signal Transducing
dc.subjectAnimals
dc.subjectAnticonvulsants
dc.subjectDisease Models, Animal
dc.subjectEpilepsy
dc.subjectHippocampus
dc.subjectHumans
dc.subjectIsoenzymes
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectKainic Acid
dc.subjectMAP Kinase Signaling System
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectMitogen-Activated Protein Kinase 10
dc.subjectNerve Degeneration
dc.titleRole of JNK isoforms in the kainic acid experimental model of epilepsy and neurodegeneration
dc.typeReview


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