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

@article{Chung2015SocialDI,
  title={Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression},
  author={Woosuk Chung and Su Yeon Choi and Eunee Lee and Haram Park and Jaeseung Kang and Hanwool Park and Yeonsoo Choi and Dongsoo Lee and Sae-Geun Park and Ryunhee Kim and Yi Sul Cho and Jeonghoon Choi and Myoung-Hwan Kim and Jong Won Lee and Seungjoon Lee and Issac Rhim and Min Whan Jung and Daesoo Kim and Yong Chul Bae and Eunjoon Kim},
  journal={Nature Neuroscience},
  year={2015},
  volume={18},
  pages={435-443}
}
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… CONTINUE READING
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