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Consequences of excessive plasticity in the hippocampus induced by perinatal asphyxia

dc.contributor.authorSaraceno G.E.
dc.contributor.authorCaceres L.G.
dc.contributor.authorGuelman L.R.
dc.contributor.authorCastilla R.
dc.contributor.authorUdovin L.D.
dc.contributor.authorEllisman M.H.
dc.contributor.authorBrocco M.A.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:28:06Z
dc.date.available2020-09-02T22:28:06Z
dc.date.issued2016
dc.identifier10.1016/j.expneurol.2016.08.017
dc.identifier.citation286, , 116-123
dc.identifier.issn00144886
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6202
dc.descriptionPerinatal asphyxia (PA) is one of the most frequent risk factors for several neurodevelopmental disorders (NDDs) of presumed multifactorial etiology. Dysfunction of neuronal connectivity is thought to play a central role in the pathophysiology of NDDs. Because underlying causes of some NDDs begin before/during birth, we asked whether this clinical condition might affect accurate establishment of neural circuits in the hippocampus as a consequence of disturbed brain plasticity. We used a murine model that mimics the pathophysiological processes of perinatal asphyxia. Histological analyses of neurons (NeuN), dendrites (MAP-2), neurofilaments (NF-M/Hp) and correlative electron microscopy studies of dendritic spines were performed in Stratum radiatum of the hippocampal CA1 area after postnatal ontogenesis. Protein and mRNA analyses were achieved by Western blot and RT-qPCR. Behavioral tests were also carried out. NeuN abnormal staining and spine density were increased. RT-qPCR assays revealed a β-actin mRNA over-expression, while Western blot analysis showed higher β-actin protein levels in synaptosomal fractions in experimental group. M6a expression, protein involved in filopodium formation and synaptogenesis, was also increased. Furthermore, we found that PI3K/Akt/GSK3 pathway signaling, which is involved in synaptogenesis, was activated. Moreover, asphyctic animals showed habituation memory changes in the open field test. Our results suggest that abnormal synaptogenesis induced by PA as a consequence of excessive brain plasticity during brain development may contribute to the etiology of the NDDs. Consequences of this altered synaptic maturation can underlie some of the later behavioral deficits observed in NDDs. © 2016
dc.language.isoen
dc.publisherAcademic Press Inc.
dc.subjectHabituation memory
dc.subjectM6a
dc.subjectNeurodevelopmental disorders
dc.subjectPI3K/Akt/GSK3 pathway
dc.subjectSynaptogenesis
dc.subjectβ-Actin
dc.subjectbeta actin
dc.subjectglycogen synthase kinase 3
dc.subjectmessenger RNA
dc.subjectmicrotubule associated protein 2
dc.subjectneurofilament M protein
dc.subjectneuron specific nuclear protein
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectmessenger RNA
dc.subjectnerve protein
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectanxiety
dc.subjectArticle
dc.subjectbrain synaptosome
dc.subjectcontrolled study
dc.subjectdendrite
dc.subjectdendritic spine
dc.subjectfemale
dc.subjecthabituation
dc.subjecthippocampal CA1 region
dc.subjecthippocampus
dc.subjectmouse
dc.subjectnerve cell
dc.subjectnerve cell plasticity
dc.subjectneurofilament
dc.subjectnonhuman
dc.subjectperinatal asphyxia
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectpyramidal nerve cell
dc.subjectrat
dc.subjectsignal transduction
dc.subjectstratum radiatum
dc.subjectsynaptogenesis
dc.subjectanalysis of variance
dc.subjectanimal
dc.subjectasphyxia
dc.subjectavoidance behavior
dc.subjectcell fractionation
dc.subjectelectron microscopy
dc.subjectexploratory behavior
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectnerve cell plasticity
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectpregnancy
dc.subjectSprague Dawley rat
dc.subjectultrastructure
dc.subjectAnalysis of Variance
dc.subjectAnimals
dc.subjectAsphyxia
dc.subjectAvoidance Learning
dc.subjectDendritic Spines
dc.subjectExploratory Behavior
dc.subjectFemale
dc.subjectHippocampus
dc.subjectMicroscopy, Electron
dc.subjectNerve Tissue Proteins
dc.subjectNeuronal Plasticity
dc.subjectPregnancy
dc.subjectPyramidal Cells
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectRNA, Messenger
dc.subjectSignal Transduction
dc.subjectSubcellular Fractions
dc.titleConsequences of excessive plasticity in the hippocampus induced by perinatal asphyxia
dc.typeArticle


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