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

doi:10.1016/j.celrep.2018.05.087

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

Department of Dentistry

Korea Advanced Institute of Science and Technology
Institute for Basic Science
Kyungpook National University

Research output: Contribution to journal › Article › peer-review

37 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 language	English
Pages (from-to)	3839-3851
Number of pages	13
Journal	Cell Reports
Volume	23
Issue number	13
DOIs	https://doi.org/10.1016/j.celrep.2018.05.087
State	Published - 26 Jun 2018

Keywords

autism
NMDA receptors
repetitive behavior
social interaction
synaptic adhesion

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10.1016/j.celrep.2018.05.087

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title = "NGL-2 Deletion Leads to Autistic-like Behaviors Responsive to NMDAR Modulation",

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.",

keywords = "autism, NMDA receptors, repetitive behavior, social interaction, synaptic adhesion",

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

year = "2018",

month = jun,

day = "26",

doi = "10.1016/j.celrep.2018.05.087",

language = "English",

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T1 - NGL-2 Deletion Leads to Autistic-like Behaviors Responsive to NMDAR Modulation

AU - Um, Seung Min

AU - Ha, Seungmin

AU - Lee, Hyejin

AU - Kim, Jihye

AU - Kim, Kyungdeok

AU - Shin, Wangyong

AU - Cho, Yi Sul

AU - Roh, Junyeop Daniel

AU - Kang, Jaeseung

AU - Yoo, Taesun

AU - Noh, Young Woo

AU - Choi, Yeonsoo

AU - Bae, Yong Chul

AU - Kim, Eunjoon

PY - 2018/6/26

Y1 - 2018/6/26

N2 - 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.

AB - 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.

KW - autism

KW - NMDA receptors

KW - repetitive behavior

KW - social interaction

KW - synaptic adhesion

UR - https://www.scopus.com/pages/publications/85048396595

U2 - 10.1016/j.celrep.2018.05.087

DO - 10.1016/j.celrep.2018.05.087

M3 - Article

C2 - 29949768

AN - SCOPUS:85048396595

SN - 2211-1247

VL - 23

SP - 3839

EP - 3851

JO - Cell Reports

JF - Cell Reports

IS - 13

ER -

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

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Keywords

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