NGL-2 Deletion Leads to Autistic-like Behaviors Responsive to NMDAR Modulation

Seung Min Um, Seungmin Ha, Hyejin Lee, Jihye Kim, Kyungdeok Kim, Wangyong Shin, Yi Sul Cho, Junyeop Daniel Roh, Jaeseung Kang, Taesun Yoo, Young Woo Noh, Yeonsoo Choi, Yong Chul Bae, Eunjoon Kim

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

NGL-2 is a postsynaptic adhesion molecule known to regulate synaptic transmission, but whether NGL-2 regulates synaptic plasticity and specific behaviors remains unknown. Um et al. find that mice lacking NGL-2 display suppressed NMDA receptor-dependent synaptic plasticity and autistic-like social deficits and repetitive behaviors that are responsive to NMDA receptor activation.

Original languageEnglish
Pages (from-to)3839-3851
Number of pages13
JournalCell Reports
Volume23
Issue number13
DOIs
StatePublished - 26 Jun 2018

Keywords

  • autism
  • NMDA receptors
  • repetitive behavior
  • social interaction
  • synaptic adhesion

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