BROWSE

Related Scientist

Shin, Wangyong's photo.

Shin, Wangyong
시냅스 뇌질환 연구단
more info

ITEM VIEW & DOWNLOAD

SALM4 negatively regulates NMDA receptor function and fear memory consolidation

Cited 0 time in webofscience Cited 0 time in scopus
18 Viewed 0 Downloaded
Title
SALM4 negatively regulates NMDA receptor function and fear memory consolidation
Author(s)
Eunkyung Lie; Yeo, Yeji; Lee, Eun-Jae; Wangyong Shin; Kyungdeok Kim; Han, Kyung Ah; Yang, Esther; Choi, Tae-Yong; Mihyun Bae; Suho Lee; Um, Seung Min; Choi, Se-Young; Kim, Hyun; Ko, Jaewon; Eunjoon Kim
Publication Date
2021-12-01
Journal
Communications Biology, v.4, no.1
Publisher
Nature Research
Abstract
© 2021, The Author(s).Many synaptic adhesion molecules positively regulate synapse development and function, but relatively little is known about negative regulation. SALM4/Lrfn3 (synaptic adhesion-like molecule 4/leucine rich repeat and fibronectin type III domain containing 3) inhibits synapse development by suppressing other SALM family proteins, but whether SALM4 also inhibits synaptic function and specific behaviors remains unclear. Here we show that SALM4-knockout (Lrfn3−/−) male mice display enhanced contextual fear memory consolidation (7-day post-training) but not acquisition or 1-day retention, and exhibit normal cued fear, spatial, and object-recognition memory. The Lrfn3−/− hippocampus show increased currents of GluN2B-containing N-methyl-d-aspartate (NMDA) receptors (GluN2B-NMDARs), but not α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors (AMPARs), which requires the presynaptic receptor tyrosine phosphatase PTPσ. Chronic treatment of Lrfn3−/− mice with fluoxetine, a selective serotonin reuptake inhibitor used to treat excessive fear memory that directly inhibits GluN2B-NMDARs, normalizes NMDAR function and contextual fear memory consolidation in Lrfn3−/− mice, although the GluN2B-specific NMDAR antagonist ifenprodil was not sufficient to reverse the enhanced fear memory consolidation. These results suggest that SALM4 suppresses excessive GluN2B-NMDAR (not AMPAR) function and fear memory consolidation (not acquisition).
URI
https://pr.ibs.re.kr/handle/8788114/10618
DOI
10.1038/s42003-021-02656-3
ISSN
2399-3642
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
Files in This Item:
There are no files associated with this item.

qrcode

  • facebook

    twitter

  • Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.
해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse