| Literature DB >> 25622145 |
Woosuk Chung1, Su Yeon Choi2, Eunee Lee3, Haram Park2, Jaeseung Kang2, Hanwool Park1, Yeonsoo Choi2, Dongsoo Lee3, Sae-Geun Park2, Ryunhee Kim2, Yi Sul Cho4, Jeonghoon Choi2, Myoung-Hwan Kim5, Jong Won Lee3, Seungjoon Lee2, Issac Rhim3, Min Whan Jung6, Daesoo Kim2, Yong Chul Bae4, Eunjoon Kim6.
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.Entities:
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Year: 2015 PMID： 25622145 DOI： 10.1038/nn.3927
Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884