Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression Highly Cited Paper

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Title
Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
Author(s)
Woosuk Chung; Su Yeon Choi; Eunee Lee; Haram Park; Jaeseung Kang; Hanwool Park; Yeonsoo Choi; Dongsoo Lee; Sae-Geun Park; Ryunhee Kim; Yi Sul Cho; Jeonghoon Choi; Myoung-Hwan Kim; Jong Won Lee; Seungjoon Lee; Issac Rhim; Min Whan Jung; Daesoo Kim; Yong Chul Bae; Eunjoon Kim
Publication Date
2015-03
Journal
NATURE NEUROSCIENCE, v.18, no.3, pp.435 - 443
Publisher
NATURE PUBLISHING GROUP
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
URI
https://pr.ibs.re.kr/handle/8788114/1814
ISSN
1097-6256
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > Journal Papers (저널논문)
Files in This Item:
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