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

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Title
NGL-2 Deletion Leads to Autistic-like Behaviors Responsive to NMDAR Modulation
Author(s)
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
Publication Date
2018-06
Journal
Cell Reports, v.23, no.13, pp.3839 - 3851
Publisher
Cell Press
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.Netrin-G ligand 2 (NGL-2)/LRRC4, implicated in autism spectrum disorders and schizophrenia, is a leucine-rich repeat-containing postsynaptic adhesion molecule that interacts intracellularly with the excitatory postsynaptic scaffolding protein PSD-95 and trans-synaptically with the presynaptic adhesion molecule netrin-G2. Functionally, NGL-2 regulates excitatory synapse development and synaptic transmission. However, whether it regulates synaptic plasticity and disease-related specific behaviors is not known. Here, we report that mice lacking NGL-2 (Lrrc4−/− mice) show suppressed N-Methyl-D-aspartate receptor (NMDAR)-dependent synaptic plasticity in the hippocampus. NGL-2 associates with NMDARs through both PSD-95-dependent and -independent mechanisms. Moreover, Lrrc4−/− mice display mild social interaction deficits and repetitive behaviors that are rapidly improved by pharmacological NMDAR activation. These results suggest that NGL-2 promotes synaptic stabilization of NMDARs, regulates NMDAR-dependent synaptic plasticity, and prevents autistic-like behaviors from developing in mice, supporting the hypothesis that NMDAR dysfunction contributes to autism spectrum disorders. © 2018 The Author(s)
URI
https://pr.ibs.re.kr/handle/8788114/5563
ISSN
2211-1247
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > Journal Papers (저널논문)
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