Evidence map›Paper›PMID 30355491›Full record

ArticleCell reports2018

The Developmental Shift of NMDA Receptor Composition Proceeds Independently of GluN2 Subunit-Specific GluN2 C-Terminal Sequences.

Sean McKay, Tomás J Ryan, Jamie McQueen, Tim Indersmitten, Katie F M Marwick, Philip Hasel, Maksym V Kopanitsa, Paul S Baxter, Marc-André Martel, Peter C Kind and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Linear ubiquitination of the NMDA receptor GluN2A subunit facilitates the GluN2B-to-GluN2A switch and synaptic maturation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. GluN3A and Excitatory Glycine Receptors in the Adult Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Review
  7. Review
  8. Synaptic memory and CaMKII.Physiological reviews · 2023
    Review
  9. Article
  10. Article
  11. S-SCAM is essential for synapse formation.Frontiers in cellular neuroscience · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Effects of N-Methyl-D-aspartate receptor (NMDAR) and CaAnnals of translational medicine · 2021
    Article
  19. Article
  20. 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

15 authors at 4 institutions in 5 countries.

Sean McKayCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; UK Dementia Research Institute at the University of Edinburgh, Chancellor's Building, Edinburgh Medical School, Edinburgh EH16 4SB, UK.
Tomás J RyanSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland; Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC, Australia.
Jamie McQueenCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; UK Dementia Research Institute at the University of Edinburgh, Chancellor's Building, Edinburgh Medical School, Edinburgh EH16 4SB, UK.
Tim IndersmittenDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Katie F M MarwickCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK.
Philip HaselCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; UK Dementia Research Institute at the University of Edinburgh, Chancellor's Building, Edinburgh Medical School, Edinburgh EH16 4SB, UK.
Maksym V KopanitsaThe Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK; UK Dementia Research Institute at Imperial College London, Hammersmith Hospital Campus, Imperial College, London W12 0NN, UK.
Paul S BaxterCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; UK Dementia Research Institute at the University of Edinburgh, Chancellor's Building, Edinburgh Medical School, Edinburgh EH16 4SB, UK.
Marc-André MartelCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK.
Peter C KindCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK.
David J A WyllieCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK.
Thomas J O'DellDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Seth G N GrantSimons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; The Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK; Centre for Clinical Brain Sciences, University of Edinburgh Chancellor's Building, Edinburgh, UK.
Giles E HardinghamCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; Simons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; UK Dementia Research Institute at the University of Edinburgh, Chancellor's Building, Edinburgh Medical School, Edinburgh EH16 4SB, UK. Electronic address: giles.hardingham@ed.ac.uk.
Noboru H KomiyamaSimons Initiative for the Developing Brain, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK; The Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK; Centre for Clinical Brain Sciences, University of Edinburgh Chancellor's Building, Edinburgh, UK. Electronic address: n.komiyama@ed.ac.uk.
University of Edinburgh · GBUniversity of California, Los Angeles · USWellcome Sanger Institute · GBUniversity of Melbourne · AU

Funding

Chief Scientist Office PCL/17/01European Research Council 695568Medical Research Council MR/K014137/1Medical Research Council MR/P006213/1
6 · The paper itself

Abstract

The GluN2 subtype (2A versus 2B) determines biophysical properties and signaling of forebrain NMDA receptors (NMDARs). During development, GluN2A becomes incorporated into previously GluN2B-dominated NMDARs. This "switch" is proposed to be driven by distinct features of GluN2 cytoplasmic C-terminal domains (CTDs), including a unique CaMKII interaction site in GluN2B that drives removal from the synapse. However, these models remain untested in the context of endogenous NMDARs. We show that, although mutating the endogenous GluN2B CaMKII site has secondary effects on GluN2B CTD phosphorylation, the developmental changes in NMDAR composition occur normally and measures of plasticity and synaptogenesis are unaffected. Moreover, the switch proceeds normally in mice that have the GluN2A CTD replaced by that of GluN2B and commences without an observable decline in GluN2B levels but is impaired by GluN2A haploinsufficiency. Thus, GluN2A expression levels, and not GluN2 subtype-specific CTD-driven events, are the overriding factor in the developmental switch in NMDAR composition.

Indexed as

Amino Acid SequenceAnimalsBinding SitesCalcium-Calmodulin-Dependent Protein Kinase Type 2Long-Term PotentiationMice, Inbred C57BLMutationNeurogenesisPhosphorylationProtein SubunitsRatsReceptors, N-Methyl-D-AspartateSynapsesTheta RhythmCalcium-Calmodulin-Dependent Protein Kinase Type 2NR2B NMDA receptorProtein SubunitsReceptors, N-Methyl-D-AspartateneurodevelopmentNMDA receptorsynaptic plasticitysynaptogenesis

Identifiers

PMID30355491
PMCPMC6218242
OpenAlexW2896317215

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.