Evidence map›Paper›PMID 29554474›Full record

ArticleExperimental neurology2018

Impaired social behaviors and minimized oxytocin signaling of the adult mice deficient in the N-methyl-d-aspartate receptor GluN3A subunit.

Jin Hwan Lee, James Ya Zhang, Zheng Zachory Wei, Shan Ping Yu

Abstract read
In one paragraph

Article in Experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Pathogenesis of sporadic Alzheimer's disease by deficiency of NMDA receptor subunit GluN3A.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  12. Review
  13. Article
  14. The roles of GluN3-containing N-methyl-D-aspartate receptor in central nerve system.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  15. Article
  16. Article
  17. Protective effects of GPR37FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  18. Article
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

4 authors.

Jin Hwan LeeDepartment of Anesthesiology, Emory University School of Medicine, Atlanta, GA 30322, USA.
James Ya ZhangDepartment of Anesthesiology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Zheng Zachory WeiDepartment of Anesthesiology, Emory University School of Medicine, Atlanta, GA 30322, USA; Center for Visual and Neurocognitive Rehabilitation, VA Medical Center, Atlanta, GA 30033, USA.
Shan Ping YuDepartment of Anesthesiology, Emory University School of Medicine, Atlanta, GA 30322, USA; Center for Visual and Neurocognitive Rehabilitation, VA Medical Center, Atlanta, GA 30033, USA. Electronic address: spyu@emory.edu.

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
Stroke Treatment by Chemically-induced HypothermiaR44NS073378 · NINDS · JT PHARMACEUTICALS, INC. · PI DIX, THOMAS A., YU, SHAN P. · 2017 to 2019
$2.9M
Stem cell transplantation therapy via intranasal delivery after strokeR01NS091585 · NINDS · EMORY UNIVERSITY · PI WEI, LING · 2016 to 2020
$1.7M
Application of optogenetics in iPS cell transplantation therapy for ischemic stroR01NS085568 · NINDS · EMORY UNIVERSITY · PI GROSS, ROBERT E, WEI, LING · 2014 to 2018
$1.7M
Stroke Treatment by Chemically-induced HypothermiaR42NS073378 · NINDS · JT PHARMACEUTICALS, INC. · PI DIX, THOMAS A., YU, SHAN P. · 2015 to 2016
$1.5M
Neuroprotection NR3A in Cultured Neurons and Ischemic NeonatesR01NS057255 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI YU, SHAN P. · 2007 to 2011
$1.1M
Stroke Treatment by Chemically-Induced HypothermiaR41NS073378 · NINDS · HALIMED PHARMACEUTICALS, INC. · PI DIX, THOMAS A., YU, SHAN P. · 2011 to 2012
$884k
Promoting axonal growth and tissue repair in stem cell therapy after strokeR21NS075338 · NINDS · EMORY UNIVERSITY · PI WEI, LING · 2011 to 2012
$426k
Protection of the Brain by Chemical HypothermiaI01RX000666 · VA · VETERANS HEALTH ADMINISTRATION · PI YU, SHAN P. · 2015 to 2016
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NIGMS NIH HHS T32 GM008169NINDS NIH HHS R01 NS057255NINDS NIH HHS R01 NS085568NINDS NIH HHS R01 NS091585NINDS NIH HHS R21 NS075338NINDS NIH HHS R41 NS073378NINDS NIH HHS R42 NS073378NINDS NIH HHS R44 NS073378RRD VA I01 RX000666
6 · The paper itself

Abstract

The N-methyl-d-aspartate receptor (NMDAR) has been implicated in the pathophysiology of neurological diseases, such as schizophrenia, autism spectrum disorders (ASD), and Alzheimer's disease (AD), whose unique clinical hallmark is a constellation of impaired social and/or cognitive behaviors. GluN3A (NR3A) is a unique inhibitory subunit in the NMDAR complex. The role of GluN3A in social behavioral activities is obscure. In this study, we sought to evaluate altered social activities in adult GluN3A knockout (KO) mice. GluN3A KO mice spent less time in reciprocal social interaction in the social interaction test compared to wild-type (WT) mice. A social approach test using a three-chamber system confirmed that mice lacking GluN3A had lower sociability and did not exhibit a preference for social novelty. GluN3A KO mice displayed abnormal food preference in the social transmission of food preference task and low social interaction activity in the five-trial social memory test, but without social memory deficits. Using a home cage monitoring system, we observed reduced social grooming behavior in GluN3A KO mice. Signaling genes that might mediate the altered social behaviors were examined in the prefrontal cortex, hippocampus, and thalamus. Among nine genes examined, the expression of the oxytocin receptor was significantly lower in the prefrontal cortex of GluN3A KO mice than that in WT mice. Oxytocin treatment rescued social activity deficits in GluN3A KO mice. These findings support a novel idea that a chronic state of moderate increases in NMDAR activities may lead to downregulation of the oxytocin signaling and impaired behavioral activities that are seen in psychiatric/neurodegenerative disorders.

Indexed as

Social BehaviorAge FactorsAnimalsGroomingHippocampusMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutOxytocinPrefrontal CortexProtein SubunitsReceptors, N-Methyl-D-AspartateReceptors, OxytocinSignal TransductionGluN3A protein, mouseOXTR protein, mouseOxytocinProtein SubunitsReceptors, N-Methyl-D-AspartateReceptors, OxytocinGluN3ANR3AOxytocin signalingSocial behaviors

Identifiers

PMID29554474
PMCPMC5955859

What OpenQuestion holds

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Registered trials

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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.