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dc.contributor.authorMurueta-Goyena A.
dc.contributor.authorOrtuzar N.
dc.contributor.authorGargiulo P.Á.
dc.contributor.authorLafuente J.V.
dc.contributor.authorBengoetxea H.
dc.date.accessioned2020-09-02T22:24:04Z
dc.date.available2020-09-02T22:24:04Z
dc.date.issued2018
dc.identifier10.1007/s12035-017-0715-z
dc.identifier.citation55, 1, 26-41
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5473
dc.descriptionPerinatal injections of N-methyl-D-aspartate (NMDA) receptor antagonist in rodents emulate some cognitive impairments and neurochemical alterations, such as decreased GABAergic (gamma aminobutyric acid) interneuron immunoreactivity, also found in schizophrenia. These features are pervasive, and developing neuroprotective or neurorestorative strategies is of special interest. In this work, we aimed to investigate if a short exposure to enriched environment (EE) in early adulthood (P55-P73) was an effective strategy to improve cognitive dysfunction and to restore interneuron expression in medial prefrontal cortex (mPFC) and hippocampus (HPC). For that purpose,we administered MK-801 intraperitoneally to Long Evans rats from postnatal days 10 to 20. Twenty-four hours after the last injection, MK-801 produced a transient decrease in spontaneous motor activity and exploration, but those abnormalities were absent at P24 and P55. The open field test on P73 manifested that EE reduced anxiety-like behavior. In addition, MK-801-treated rats showed cognitive impairment in novel object recognition test that was reversed by EE. We quantified different interneuron populations based on their calcium-binding protein expression (parvalbumin, calretinin, and calbindin), glutamic acid decarboxylase 67, and neuronal nuclei-positive cells by means of unbiased stereology and found that EE enhanced interneuron immunoreactivity up to normal values in MK- 801-treated rats. Our results demonstrate that a timely intervention with EE is a powerful tool to reverse long-lasting changes in cognition and neurochemical markers of interneurons in an animal model of schizophrenia. © Springer Science+Business Media, LLC 2017.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectCalcium-binding proteins
dc.subjectCognitive dysfunction
dc.subjectEnriched environment
dc.subjectInterneurons
dc.subjectMK-801
dc.subject4 aminobutyric acid
dc.subjectcalbindin
dc.subjectcalretinin
dc.subjectdizocilpine
dc.subjectglutamate decarboxylase 67
dc.subjectparvalbumin
dc.subject4 aminobutyric acid receptor
dc.subjectamino acid receptor blocking agent
dc.subjectdizocilpine maleate
dc.subjectadult
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectanxiety
dc.subjectArticle
dc.subjectcognition
dc.subjectcognitive defect
dc.subjectcontrolled study
dc.subjectenvironmental enrichment
dc.subjectenvironmental exposure
dc.subjectexploratory behavior
dc.subjectfemale
dc.subjectGABAergic system
dc.subjecthippocampus
dc.subjectimmunoreactivity
dc.subjectmale
dc.subjectmedial prefrontal cortex
dc.subjectmotor activity
dc.subjectnonhuman
dc.subjectnovel object recognition test
dc.subjectopen field test
dc.subjectperinatal period
dc.subjectprotein expression
dc.subjectrat
dc.subjectschizophrenia
dc.subjectstereology
dc.subjectage
dc.subjectanimal
dc.subjectchemically induced
dc.subjectcognitive defect
dc.subjectdrug effect
dc.subjectenvironment
dc.subjectinterneuron
dc.subjectLong Evans rat
dc.subjectmetabolism
dc.subjectnewborn
dc.subjectpathology
dc.subjecttime factor
dc.subjectAge Factors
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectCognitive Dysfunction
dc.subjectDizocilpine Maleate
dc.subjectEnvironment
dc.subjectExcitatory Amino Acid Antagonists
dc.subjectFemale
dc.subjectGABAergic Neurons
dc.subjectInterneurons
dc.subjectMale
dc.subjectRats
dc.subjectRats, Long-Evans
dc.subjectTime Factors
dc.titleShort-term exposure to enriched environment in adult rats restores MK-801-induced cognitive deficits and gabaergic interneuron immunoreactivity loss
dc.typeArticle


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