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dc.contributor.authorMurueta-Goyena A.
dc.contributor.authorMorera-Herreras T.
dc.contributor.authorMiguelez C.
dc.contributor.authorGutiérrez-Ceballos A.
dc.contributor.authorUgedo L.
dc.contributor.authorLafuente J.V.
dc.contributor.authorBengoetxea H.
dc.date.accessioned2020-09-02T22:24:16Z
dc.date.available2020-09-02T22:24:16Z
dc.date.issued2019
dc.identifier10.1016/j.euroneuro.2019.03.009
dc.identifier.citation29, 5, 590-600
dc.identifier.issn0924977X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5559
dc.descriptionSchizophrenia is a mental disorder characterized by psychosis, negative symptoms and cognitive impairment. Cognitive deficits are enduring and represent the most disabling symptom but are currently poorly treated. N-methyl D-aspartate receptor (NMDAR) hypofunction hypothesis has been notably successful in explaining the pathophysiological findings and symptomatology of schizophrenia. Thereby, NMDAR blockade in rodents represents a useful tool to identify new therapeutic approaches. In this regard, enriched environment (EE) could play an essential role. Using a multilevel approach of behavior, electrophysiology and protein analysis, we showed that a short-term exposure to EE in adulthood ameliorated spatial learning and object-place associative memory impairment observed in postnatally MK-801-treated Long Evans rats. Moreover, EE in adult life restored long-term potentiation (LTP) in hippocampal-medial prefrontal pathway abolished by MK-801 treatment. EE in adulthood also induced a set of modifications in the expression of proteins related to glutamatergic neurotransmission. Taken together, these findings shed new light on the neurobiological effects of EE to reverse the actions of MK-801 and offer a preclinical testing of a therapeutic strategy that may be remarkably effective for managing cognitive symptoms of schizophrenia. © 2019
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAssociative memory
dc.subjectElectrophysiology
dc.subjectGlutamate receptor
dc.subjectNeurodevelopmental disorder
dc.subjectSpatial learning
dc.subjectdizocilpine
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectamino acid receptor blocking agent
dc.subjectdizocilpine maleate
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectadulthood
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectassociative memory
dc.subjectbehavior assessment
dc.subjectcognition
dc.subjectelectrophysiology
dc.subjectenvironmental enrichment
dc.subjecthippocampus
dc.subjectLong Evans rat
dc.subjectlong term potentiation
dc.subjectmedial prefrontal cortex
dc.subjectmemory disorder
dc.subjectnerve cell plasticity
dc.subjectnonhuman
dc.subjectperinatal period
dc.subjectpriority journal
dc.subjectprotein analysis
dc.subjectprotein expression
dc.subjectrat
dc.subjectschizophrenia
dc.subjectspatial learning
dc.subjectage
dc.subjectanimal
dc.subjectbiosynthesis
dc.subjectcognition
dc.subjectdrug effect
dc.subjectenvironment
dc.subjectgene expression
dc.subjectgenetics
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectnerve cell plasticity
dc.subjectnerve tract
dc.subjectphysiology
dc.subjectprefrontal cortex
dc.subjectschizophrenia
dc.subjectAge Factors
dc.subjectAnimals
dc.subjectCognition
dc.subjectDizocilpine Maleate
dc.subjectEnvironment
dc.subjectExcitatory Amino Acid Antagonists
dc.subjectGene Expression
dc.subjectHippocampus
dc.subjectNeural Pathways
dc.subjectNeuronal Plasticity
dc.subjectPrefrontal Cortex
dc.subjectRats
dc.subjectRats, Long-Evans
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectSchizophrenia
dc.titleEffects of adult enriched environment on cognition, hippocampal-prefrontal plasticity and NMDAR subunit expression in MK-801-induced schizophrenia model
dc.typeArticle


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