期刊
NEURON
卷 89, 期 1, 页码 163-176出版社
CELL PRESS
DOI: 10.1016/j.neuron.2015.11.036
关键词
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资金
- CNRS ATIP-Avenir
- Agence Nationale de la Recherche [ANR-12-BSV4-0021-01, ANR-13-JSV4-0002-01]
- Ville de Paris
- NIH [R01MH097879]
- Agence Nationale de la Recherche (ANR) [ANR-12-BSV4-0021, ANR-13-JSV4-0002] Funding Source: Agence Nationale de la Recherche (ANR)
Several neuropsychiatric disorders are associated with cognitive and social dysfunction. Postmortem studies of patients with schizophrenia have revealed specific changes in area CA2, a long-overlooked region of the hippocampus recently found to be critical for social memory formation. To examine how area CA2 is altered in psychiatric illness, we used the Df(16)A(+/-) mouse model of the 22q11.2 microdeletion, a genetic risk factor for developing several neuropsychiatric disorders, including schizophrenia. We report several age-dependent CA2 alterations: a decrease in the density of parvalbumin-expressing interneurons, a reduction in the amount of feedforward inhibition, and a change in CA2 pyramidal-neuron intrinsic properties. Furthermore, we found that area CA2 is less plastic in Df(16) A(+/-) mice, making it nearly impossible to evoke action potential firing in CA2 pyramidal neurons. Finally, we show that Df(16) A(+/-) mice display impaired social cognition, providing a potential mechanism and a neural substrate for this impairment in psychiatric disorders.
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