한빛사 논문
Abstract
Woosuk Chung1,7, Su Yeon Choi2,7, Eunee Lee3,7, Haram Park2,7, Jaeseung Kang2, Hanwool Park1, Yeonsoo Choi2, Dongsoo Lee3, Sae-Geun Park2, Ryunhee Kim2, Yi Sul Cho4, Jeonghoon Choi2, Myoung-Hwan Kim5,6, Jong Won Lee3, Seungjoon Lee2, Issac Rhim3, Min Whan Jung2,3, Daesoo Kim2, Yong Chul Bae4 & Eunjoon Kim2,3
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea. 2Department of Biological Sciences, KAIST, Daejeon, Korea. 3Center for Synaptic Brain Dysfunctions, Institute for Basic Science, Daejeon, Korea. 4Department of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu, Korea. 5Department of Physiology, Seoul National University College of Medicine, Seoul, Korea. 6Seoul National University Bundang Hospital, Gyeonggi, Korea. 7These authors contributed equally to this work.
Correspondence to: Eunjoon Kim
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.
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