Evidence map›Paper›PMID 34588597›Full record

ArticleCommunications biology2021

SALM4 negatively regulates NMDA receptor function and fear memory consolidation.

Eunkyung Lie, Yeji Yeo, Eun-Jae Lee, Wangyong Shin, Kyungdeok Kim, Kyung Ah Han, Esther Yang, Tae-Yong Choi, Mihyun Bae, Suho Lee and 5 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Acetazolamide inhibition of carbonic anhydrase 4 reverses opioid-induced synaptic rearrangements in nucleus accumbens and reduces drug-seeking behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 1 country.

Eunkyung LieCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Yeji YeoDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.
Eun-Jae LeeDepartment of Neurology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, 05505, Korea.
Wangyong ShinCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.ORCID http://orcid.org/0000-0003-3227-8405
Kyungdeok KimCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Kyung Ah HanDepartment of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Hyeonpoong-Eup, Dalseong-Gun, Daegu, 42988, Korea.
Esther YangDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University, Seoul, 02841, Korea.
Tae-Yong ChoiDepartment of Physiology and Neuroscience, Dental Research Institute, Seoul National University School of Dentistry, Seoul, 03080, Korea.
Mihyun BaeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Suho LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Seung Min UmDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.
Se-Young ChoiDepartment of Physiology and Neuroscience, Dental Research Institute, Seoul National University School of Dentistry, Seoul, 03080, Korea.ORCID http://orcid.org/0000-0001-7534-5167
Hyun KimDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University, Seoul, 02841, Korea.
Jaewon KoDepartment of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Hyeonpoong-Eup, Dalseong-Gun, Daegu, 42988, Korea.
Eunjoon KimCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea. kime@kaist.ac.kr.ORCID http://orcid.org/0000-0001-5518-6584
Institute for Basic Science · KRDaegu Gyeongbuk Institute of Science and Technology · KRKorea Advanced Institute of Science and Technology · KRKorea University · KRSeoul National University · KRUlsan College · KRDongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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

Indexed as

AnimalsCell Adhesion Molecules, NeuronalFearMemory ConsolidationMiceMice, KnockoutReceptors, N-Methyl-D-AspartateCell Adhesion Molecules, NeuronalLrfn3 protein, mouseNR2B NMDA receptorReceptors, N-Methyl-D-Aspartate

Identifiers

PMID34588597
PMCPMC8481232
OpenAlexW3204484799

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.