Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression.
Nat Neurosci
; 18(3): 435-43, 2015 Mar.
Article
em En
| MEDLINE
| ID: mdl-25622145
ABSTRACT
Social deficits are observed in diverse psychiatric disorders, including autism spectrum disorders and schizophrenia. We found that mice lacking the excitatory synaptic signaling scaffold IRSp53 (also known as BAIAP2) showed impaired social interaction and communication. Treatment of IRSp53(-/-) mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist that indirectly inhibits NMDAR function, normalized social interaction. This social rescue was accompanied by normalization of NMDAR function and plasticity in the hippocampus and neuronal firing in the medial prefrontal cortex. These results, together with the reduced NMDAR function implicated in social impairments, suggest that deviation of NMDAR function in either direction leads to social deficits and that correcting the deviation has beneficial effects.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Transtornos do Comportamento Social
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Regulação da Expressão Gênica
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Receptores de N-Metil-D-Aspartato
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Receptor de Glutamato Metabotrópico 5
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Mutação
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Proteínas do Tecido Nervoso
Tipo de estudo:
Observational_studies
Limite:
Animals
Idioma:
En
Revista:
Nat Neurosci
Assunto da revista:
NEUROLOGIA
Ano de publicação:
2015
Tipo de documento:
Article