Evidence map›Paper›PMID 31291571›Full record

ArticleCell reports2019

NMDAR-Activated PP1 Dephosphorylates GluN2B to Modulate NMDAR Synaptic Content.

Andrew M Chiu, Jiejie Wang, Michael P Fiske, Pavla Hubalkova, Levi Barse, John A Gray, Antonio Sanz-Clemente

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  10. NMDARs in Alzheimer's Disease: Between Synaptic and Extrasynaptic Membranes.International journal of molecular sciences · 2024
    Review
  11. Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  12. Review
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  19. Regulation of Synaptic Transmission and Plasticity by Protein Phosphatase 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  20. Review
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.

Andrew M ChiuDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Jiejie WangDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Michael P FiskeDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Pavla HubalkovaDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Cellular Neurophysiology, Institute of Physiology CAS, Prague 142 20, Czech Republic.
Levi BarseDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
John A GrayCenter for Neuroscience, University of California, Davis, Davis, CA 95618, USA.
Antonio Sanz-ClementeDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: antonio.sanz-clemente@northwestern.edu.
Northwestern University · USUniversity of California, Davis · US

Funding

CELLULAR &MOLECULAR BASIS OF DISEASE TRAINING PROGRAMT32GM008061 · NIGMS · NORTHWESTERN UNIVERSITY · PI CARTHEW, RICHARD W. · 1985 to 2022
$17.1M
Role of CK2 in NMDAR trafficking during development and in Alzheimer's diseaseR00AG041225 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SANZ-CLEMENTE, ANTONIO · 2015 to 2017
$747k
Synaptic targeting and regulation of NMDAR subunitsK08MH100562 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRAY, JOHN ALAN · 2013 to 2016
$723k
NIA NIH HHS K99 AG041225NIA NIH HHS R00 AG041225NIGMS NIH HHS T32 GM008061NIMH NIH HHS K08 MH100562
6 · The paper itself

Abstract

In mature neurons, postsynaptic N-methyl-D-aspartate receptors (NMDARs) are segregated into two populations, synaptic and extrasynaptic, which differ in localization, function, and associated intracellular cascades. These two pools are connected via lateral diffusion, and receptor exchange between them modulates synaptic NMDAR content. Here, we identify the phosphorylation of the PDZ-ligand of the GluN2B subunit of NMDARs (at S1480) as a critical determinant in dynamically controlling NMDAR synaptic content. We find that phosphorylation of GluN2B at S1480 maintains NMDARs at extrasynaptic membranes as part of a protein complex containing protein phosphatase 1 (PP1). Global activation of NMDARs leads to the activation of PP1, which mediates dephosphorylation of GluN2B at S1480 to promote an increase in synaptic NMDAR content. Thus, PP1-mediated dephosphorylation of the GluN2B PDZ-ligand modulates the synaptic expression of NMDARs in mature neurons in an activity-dependent manner, a process with profound consequences for synaptic and structural plasticity, metaplasticity, and synaptic neurotransmission.

Indexed as

AnimalsCells, CulturedFemaleLigandsMaleMiceMice, Inbred C57BLNeuronsPDZ DomainsPhosphorylationProtein Phosphatase 1RatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSynapsesLigandsNR2B NMDA receptorProtein Phosphatase 1Receptors, N-Methyl-D-Aspartatedephosphorylationextrasynaptic NMDARGluN2BNMDA receptorsNMDAR synaptic contentPP1

Identifiers

PMID31291571
PMCPMC6639021
OpenAlexW2962482112

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.