Mostrar el registro sencillo del ítem
dc.contributor.author
Belforte, Juan Emilio
dc.contributor.author
Zsiros, Veronika
dc.contributor.author
Sklar, Elyse R
dc.contributor.author
Jiang, Zhihong
dc.contributor.author
Yu, Gu
dc.contributor.author
Li, Yuqing
dc.contributor.author
Quinlan, Elizabeth M
dc.contributor.author
Nakazawa, Kazu
dc.date.available
2020-01-29T20:50:34Z
dc.date.issued
2009-11
dc.identifier.citation
Belforte, Juan Emilio; Zsiros, Veronika; Sklar, Elyse R; Jiang, Zhihong; Yu, Gu; et al.; Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes; Nature Publishing Group; Nature Neuroscience.; 13; 1; 11-2009; 76-83
dc.identifier.issn
1097-6256
dc.identifier.uri
http://hdl.handle.net/11336/96174
dc.description.abstract
Cortical GABAergic dysfunction may underlie the pathophysiology of psychiatric disorders, including schizophrenia. Here, we characterized a mouse strain in which the essential NR1 subunit of the NMDA receptor (NMDAR) was selectively eliminated in 40–50% of cortical and hippocampal interneurons in early postnatal development. Consistent with the NMDAR hypofunction theory of schizophrenia, distinct schizophrenia-related symptoms emerged after adolescence, including novelty-induced hyperlocomotion, mating and nest-building deficits, as well as anhedonia-like and anxiety-like behaviors. Many of these behaviors were exacerbated by social isolation stress. Social memory, spatial working memory and prepulse inhibition were also impaired. Reduced expression of glutamic acid decarboxylase 67 and parvalbumin was accompanied by disinhibition of cortical excitatory neurons and reduced neuronal synchrony. Postadolescent deletion of NR1 did not result in such abnormalities. These findings suggest that early postnatal inhibition of NMDAR activity in corticolimbic GABAergic interneurons contributes to the pathophysiology of schizophrenia-related disorders.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Nature Publishing Group
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
esquizofrenia
dc.subject
nmda
dc.subject
interneuronas
dc.subject.classification
Otras Ciencias Médicas
dc.subject.classification
Otras Ciencias Médicas
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-01-29T15:43:08Z
dc.journal.volume
13
dc.journal.number
1
dc.journal.pagination
76-83
dc.journal.pais
Reino Unido
dc.journal.ciudad
Londres
dc.description.fil
Fil: Belforte, Juan Emilio. Wayne State University; Estados Unidos. National Institute of Mental Health; Estados Unidos. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Zsiros, Veronika. National Institute of Mental Health; Estados Unidos
dc.description.fil
Fil: Sklar, Elyse R. National Institute of Mental Health; Estados Unidos. Wayne State University; Estados Unidos
dc.description.fil
Fil: Jiang, Zhihong. National Institute of Mental Health; Estados Unidos
dc.description.fil
Fil: Yu, Gu. University of Maryland; Estados Unidos
dc.description.fil
Fil: Li, Yuqing. University of Alabama at Birmingahm; Estados Unidos
dc.description.fil
Fil: Quinlan, Elizabeth M. University of Maryland; Estados Unidos
dc.description.fil
Fil: Nakazawa, Kazu. National Institute of Mental Health; Estados Unidos
dc.journal.title
Nature Neuroscience.
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797836/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1038%2Fnn.2447
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/nn.2447
Archivos asociados