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dc.contributor.authorFuentealba C.R.
dc.contributor.authorFiedler J.L.
dc.contributor.authorPeralta F.A.
dc.contributor.authorAvalos A.M.
dc.contributor.authorAguayo F.I.
dc.contributor.authorMorgado-Gallardo K.P.
dc.contributor.authorAliaga E.E.
dc.date.accessioned2020-09-02T22:18:01Z
dc.date.available2020-09-02T22:18:01Z
dc.date.issued2019
dc.identifier10.3389/fnmol.2019.00261
dc.identifier.citation12, , -
dc.identifier.issn16625099
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4530
dc.descriptionAutism is a neurodevelopmental disorder characterized by a deep deficit in language and social interaction, accompanied by restricted, stereotyped and repetitive behaviors. The use of genetic autism animal models has revealed that the alteration of the mechanisms controlling the formation and maturation of neural circuits are points of convergence for the physiopathological pathways in several types of autism. Brain Derived Neurotrophic Factor (BDNF), a key multifunctional regulator of brain development, has been related to autism in several ways. However, its precise role is still elusive, in part, due to its extremely complex posttranscriptional regulation. In order to contribute to this topic, we treated prenatal rats with Valproate, a well-validated model of autism, to analyze BDNF levels in the hippocampus of juvenile rats. Valproate-treated rats exhibited an autism-like behavioral profile, characterized by a deficit in social interaction, anxiety-like behavior and repetitive behavior. In situ hybridization (ISH) experiments revealed that Valproate reduced BDNF mRNA, especially long-3′UTR-containing transcripts, in specific areas of the dentate gyrus (DG) and CA3 regions. At the same time, Valproate reduced BDNF immunoreactivity in the suprapyramidal and lucidum layers of CA3, but improved hippocampus-dependent spatial learning. The molecular changes reported here may help to explain the cognitive and behavioral signs of autism and reinforce BDNF as a potential molecular target for this neurodevelopmental disorder. © Copyright © 2019 Fuentealba, Fiedler, Peralta, Avalos, Aguayo, Morgado-Gallardo and Aliaga.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectautism
dc.subjectBDNF
dc.subjecthippocampus
dc.subjectlong-3′UTR-bdnf
dc.subjectvalproate
dc.subjectbrain derived neurotrophic factor
dc.subjectvalproic acid
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectanxiety
dc.subjectArticle
dc.subjectautism
dc.subjectcompulsion
dc.subjectcontrolled study
dc.subjectdentate gyrus
dc.subjectexperimental behavioral test
dc.subjecthippocampus
dc.subjectimmunohistochemistry
dc.subjectimmunoreactivity
dc.subjectin situ hybridization
dc.subjectjuvenile
dc.subjectmemory
dc.subjectnonhuman
dc.subjectprenatal period
dc.subjectrat
dc.subjectRNA probe
dc.subjectsocial interaction
dc.subjectspatial memory
dc.subjectspatial memory test
dc.subjecttranscription regulation
dc.subjectY-maze test
dc.titleRegion-Specific Reduction of BDNF Protein and Transcripts in the Hippocampus of Juvenile Rats Prenatally Treated With Sodium Valproate
dc.typeArticle


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