Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-01

AUTHORS

Juan E Belforte, Veronika Zsiros, Elyse R Sklar, Zhihong Jiang, Gu Yu, Yuqing Li, Elizabeth M Quinlan, Kazu Nakazawa

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. More... »

PAGES

76-83

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nn.2447

    DOI

    http://dx.doi.org/10.1038/nn.2447

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1039762019

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/19915563


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