Evidence map›Paper›PMID 25429143›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

GluN2B-containing NMDA receptors promote glutamate synapse development in hippocampal interneurons.

Wolfgang Kelsch, Zhijun Li, Sebastian Wieland, Oleg Senkov, Anne Herb, Christina Göngrich, Hannah Monyer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Proceedings of the National Academy of Sciences of the United States of America · 2026
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  13. The ontogeny of memory persistence and specificity.Developmental cognitive neuroscience · 2019
    Review
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  18. Enhanced susceptibility of CA3 hippocampus to prenatal nicotine exposure.Journal of developmental origins of health and disease · 2017
    Article
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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

7 authors at 2 institutions in 2 countries.

Wolfgang KelschCentral Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, 68159 Mannheim, Germany.ORCID http://orcid.org/0000-0002-3470-8125
Zhijun LiDepartment of Clinical Neurobiology, Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Sebastian WielandCentral Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, 68159 Mannheim, Germany.
Oleg SenkovDepartment of Clinical Neurobiology, Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany, Molecular Neuroplasticity Group, DZNE, 39120 Magdeburg, Germany, and.
Anne HerbDepartment of Clinical Neurobiology, Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Christina GöngrichDepartment of Clinical Neurobiology, Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany, Department of Neuroscience, Karolinska Institute, 171 77 Stockholm, Sweden.
Hannah MonyerDepartment of Clinical Neurobiology, Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany, h.monyer@dkfz-heidelberg.de.
German Cancer Research Center · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In postnatal development, GluN2B-containing NMDARs are critical for the functional maturation of glutamatergic synapses. GluN2B-containing NMDARs prevail until the second postnatal week when GluN2A subunits are progressively added, conferring mature properties to NMDARs. In cortical principal neurons, deletion of GluN2B results in an increase in functional AMPAR synapses, suggesting that GluN2B-containing NMDARs set a brake on glutamate synapse maturation. The function of GluN2B in the maturation of glutamatergic inputs to cortical interneurons is not known. To examine the function of GluN2B in interneurons, we generated mutant mice with conditional deletion of GluN2B in interneurons (GluN2B(ΔGAD67)). In GluN2B(ΔGAD67) mice interneurons distributed normally in cortical brain regions. After the second postnatal week, GluN2B(ΔGAD67) mice developed hippocampal seizures and died shortly thereafter. Before the onset of seizures, GluN2B-deficient hippocampal interneurons received fewer glutamatergic synaptic inputs than littermate controls, indicating that GluN2B-containing NMDARs positively regulate the maturation of glutamatergic input synapses in interneurons. These findings suggest that GluN2B-containing NMDARs keep the circuit activity under control by promoting the maturation of excitatory synapses in interneurons.

Indexed as

AnimalsAnimals, NewbornFemaleGene Knock-In TechniquesGlutamic AcidHippocampusInterneuronsMaleMiceMice, Inbred C57BLMice, KnockoutOrgan Culture TechniquesReceptors, N-Methyl-D-AspartateSynapsesGlutamic AcidNR2B NMDA receptorReceptors, N-Methyl-D-AspartateGluN2BhippocampusinterneuronsNMDARspostnatal developmentseizures

Identifiers

PMID25429143
PMCPMC6608474
OpenAlexW2027952422

What OpenQuestion holds

Textmetadata
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.