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JNK Isoforms Are Involved in the Control of Adult Hippocampal Neurogenesis in Mice, Both in Physiological Conditions and in an Experimental Model of Temporal Lobe Epilepsy

dc.contributor.authorCastro-Torres R.D.
dc.contributor.authorLanda J.
dc.contributor.authorRabaza M.
dc.contributor.authorBusquets O.
dc.contributor.authorOlloquequi J.
dc.contributor.authorEttcheto M.
dc.contributor.authorBeas-Zarate C.
dc.contributor.authorFolch J.
dc.contributor.authorCamins A.
dc.contributor.authorAuladell C.
dc.contributor.authorVerdaguer E.
dc.date.accessioned2020-09-02T22:14:45Z
dc.date.available2020-09-02T22:14:45Z
dc.date.issued2019
dc.identifier10.1007/s12035-019-1476-7
dc.identifier.citation56, 8, 5856-5865
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3970
dc.descriptionNeurogenesis in the adult dentate gyrus (DG) of the hippocampus allows the continuous generation of new neurons. This cellular process can be disturbed under specific environmental conditions, such as epileptic seizures; however, the underlying mechanisms responsible for their control remain largely unknown. Although different studies have linked the JNK (c-Jun-N-terminal-kinase) activity with the regulation of cell proliferation and differentiation, the specific function of JNK in controlling adult hippocampal neurogenesis is not well known. The purpose of this study was to analyze the role of JNK isoforms (JNK1/JNK2/JNK3) in adult-hippocampal neurogenesis. To achieve this goal, we used JNK-knockout mice (Jnk1−/−, Jnk2−/−, and Jnk3−/−), untreated and treated with intraperitoneal injections of kainic acid (KA), as an experimental model of epilepsy. In each condition, we identified cell subpopulations at different stages of neuronal maturation by immunohistochemical specific markers. In physiological conditions, we evidenced that JNK1 and JNK3 control the levels of one subtype of early progenitor cells (GFAP+/Sox2+) but not the GFAP+/Nestin+ cell subtype. Moreover, the absence of JNK1 induces an increase of immature neurons (Doublecortin+; PSA-NCAM+ cells) compared with wild-type (WT). On the other hand, Jnk1−/− and Jnk3−/− mice showed an increased capacity to maintain hippocampal homeostasis, since calbindin immunoreactivity is higher than in WT. An important fact is that, after KA injection, Jnk1−/− and Jnk3−/− mice show no increase in the different neurogenic cell subpopulation analyzed, in contrast to what occurs in WT and Jnk2−/− mice. All these data support that JNK isoforms are involved in the adult neurogenesis control. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAdult hippocampal neurogenesis
dc.subjectJNK isoforms
dc.subjectKainic acid
dc.subjectKnockout mice
dc.subjectcalbindin
dc.subjectdoublecortin
dc.subjectkainic acid
dc.subjectmitogen activated protein kinase 12
dc.subjectmitogen activated protein kinase p38
dc.subjectnestin
dc.subjectstress activated protein kinase
dc.subjectstress activated protein kinase 1
dc.subjecttranscription factor Sox2
dc.subjectcalbindin
dc.subjectglial fibrillary acidic protein
dc.subjectisoenzyme
dc.subjectkainic acid
dc.subjectnerve cell adhesion molecule L1
dc.subjectnestin
dc.subjectpolysialyl neural cell adhesion molecule
dc.subjectsialic acid derivative
dc.subjectstress activated protein kinase
dc.subjecttranscription factor Sox
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectcell maturation
dc.subjectcell subpopulation
dc.subjectcontrolled study
dc.subjecthomeostasis
dc.subjectimmunocompetent cell
dc.subjectimmunohistochemistry
dc.subjectimmunoreactivity
dc.subjectknockout mouse
dc.subjectmouse
dc.subjectnerve cell
dc.subjectnervous system development
dc.subjectnonhuman
dc.subjecttemporal lobe epilepsy
dc.subjectaging
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectcell count
dc.subjectdentate gyrus
dc.subjectdisease model
dc.subjectenzymology
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectneural stem cell
dc.subjectpathology
dc.subjecttemporal lobe epilepsy
dc.subjectAging
dc.subjectAnimals
dc.subjectCalbindins
dc.subjectCell Count
dc.subjectDentate Gyrus
dc.subjectDisease Models, Animal
dc.subjectEpilepsy, Temporal Lobe
dc.subjectGlial Fibrillary Acidic Protein
dc.subjectHippocampus
dc.subjectIsoenzymes
dc.subjectJNK Mitogen-Activated Protein Kinases
dc.subjectKainic Acid
dc.subjectMice, Inbred C57BL
dc.subjectNestin
dc.subjectNeural Cell Adhesion Molecule L1
dc.subjectNeural Stem Cells
dc.subjectNeurogenesis
dc.subjectNeurons
dc.subjectSialic Acids
dc.subjectSOXB1 Transcription Factors
dc.titleJNK Isoforms Are Involved in the Control of Adult Hippocampal Neurogenesis in Mice, Both in Physiological Conditions and in an Experimental Model of Temporal Lobe Epilepsy
dc.typeArticle


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