Evidence map›Paper›PMID 31508206›Full record

ReviewF1000Research2019

NMDA receptor C-terminal signaling in development, plasticity, and disease.

Giles Hardingham

Abstract readReview
In one paragraph

Review in F1000Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–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

23 citing papers in PubMed.

  1. Article
  2. Article
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  4. TargetingInternational journal of molecular sciences · 2024
    Review
  5. Article
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  7. Article
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  9. Article
  10. Review
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  14. Review
  15. Article
  16. Palmitoylation Controls NMDA Receptor Function and Steroid Sensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  17. Article
  18. Review
  19. Review
  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

1 author.

Giles HardinghamUK Dementia Research Institute, University of Edinburgh, Edinburgh, EH16 4TJ, UK.ORCID 0000-0002-7629-5314

Funding

Medical Research Council
6 · The paper itself

Abstract

The NMDA subtype of ionotropic glutamate receptor is a sophisticated integrator and transducer of information. NMDAR-mediated signals control diverse processes across the life course, including synaptogenesis and synaptic plasticity, as well as contribute to excitotoxic processes in neurological disorders. At the basic biophysical level, the NMDAR is a coincidence detector, requiring the co-presence of agonist, co-agonist, and membrane depolarization in order to open. However, the NMDAR is not merely a conduit for ions to flow through; it is linked on the cytoplasmic side to a large network of signaling and scaffolding proteins, primarily via the C-terminal domain of NMDAR GluN2 subunits. These physical interactions help to organize the signaling cascades downstream of NMDAR activation. Notably, the NMDAR does not come in a single form: the subunit composition of the NMDAR, particularly the GluN2 subunit subtype (GluN2A-D), influences the biophysical properties of the channel. Moreover, a growing number of studies have illuminated the extent to which GluN2 C-terminal interactions vary according to GluN2 subtype and how this impacts on the processes that NMDAR activity controls. We will review recent advances, controversies, and outstanding questions in this active area of research.

Indexed as

Neuronal PlasticitySignal TransductionHumansNervous System DiseasesNeurogenesisProtein SubunitsReceptors, N-Methyl-D-AspartateProtein SubunitsReceptors, N-Methyl-D-AspartateCalciumDevelopmentExcitotoxicityNeurodegenerationNMDA ReceptorPlasticity

Identifiers

PMID31508206
PMCPMC6720038

What OpenQuestion holds

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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.