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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

1 Jan 2017Review

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

Carme Auladell 1,4,10, Luisa de Lemos 2, Ester Verdaguer 1,4,10, Miren Ettcheto 3,4, Oriol Busquets 3,4, Alberto Lazarowski 6, Carlos Beas-Zarate 7,8, Jordi Olloquequi 9, Jaume Folch 3,5, Antoni Camins 3,4,10,*
Affiliations
Article Info

1 Departament de Biologia Cellular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain

2 Instituto Gulbenkian de Ciencia, Rua Quinta Grande 6,2780-156 Oeiras, Portugal

3 Unitat de Farmacologia i Farmacognosia, Facultat de Farmacia, Universitat de Barcelona, Barcelona, Spain

4 Biomedical Research Networking Center in Neurodegenerative Diseases (CIBERNED), Madrid, Spain

5 Unitat de Bioquimica i Biotecnologia, Facultat de Medicina i Ciencies de la Salut, Universitat Rovira i Virgili, Reus, Tarragona, Spain

6 Instituto de Investigaciones en Fisiopatologia y Bioquimica Clinica (INFIBIOC), Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina

7 Departamento de Biología Celular y Molecular, C.U.C.B.A., Universidad de Guadalajara and Division de Neurociencias, Sierra Mojada 800, Col. Independencia, Guadalajara, Jalisco 44340, Mexico

8 Centro de Investigacion Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Jalisco 44340, Mexico

9 Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Talca, Chile

10 Institute of Neurosciences, University of Barcelona, Spain

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.

Keywords

  • Kainic Acid
  • HippocampuS
  • c-Jun N-Terminal Kinase Signaling Pathway
  • Apoptosis
  • Neuroprotection
  • Review

References