Evidence map›Paper›PMID 33533533›Full record

ArticleThe Journal of physiology2021

Ca

Stuart G Cull-Candy, Mark Farrant

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  6. Review
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  10. Review
  11. Article
  12. Functional CaScientific reports · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Neuron-glioma synaptic transmission amplified by free 19S proteasome-mediated AMPAR deubiquitination promotes tumor progression.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  17. Article
  18. Article
  19. Article
  20. Review

7 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Stuart G Cull-CandyDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, UK.ORCID 0000-0002-0831-8326
Mark FarrantDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, UK.ORCID 0000-0002-9918-0376
University College London · GB

Funding

Medical Research Council MR/J002976/1Medical Research Council MR/T002506/1
6 · The paper itself

Abstract

AMPA receptors are tetrameric glutamate-gated ion channels that mediate a majority of fast excitatory neurotransmission in the brain. They exist as calcium-impermeable (CI-) and calcium-permeable (CP-) subtypes, the latter of which lacks the GluA2 subunit. CP-AMPARs display an array of distinctive biophysical and pharmacological properties that allow them to be functionally identified. This has revealed that they play crucial roles in diverse forms of central synaptic plasticity. Here we summarise the functional hallmarks of CP-AMPARs and describe how these are modified by the presence of auxiliary subunits that have emerged as pivotal regulators of AMPARs. A lasting change in the prevalence of GluA2-containing AMPARs, and hence in the fraction of CP-AMPARs, is a feature in many maladaptive forms of synaptic plasticity and neurological disorders. These include modifications of glutamatergic transmission induced by inflammatory pain, fear conditioning, cocaine exposure, and anoxia-induced damage in neurons and glia. Furthermore, defective RNA editing of GluA2 can cause altered expression of CP-AMPARs and is implicated in motor neuron damage (amyotrophic lateral sclerosis) and the proliferation of cells in malignant gliomas. A number of the players involved in CP-AMPAR regulation have been identified, providing useful insight into interventions that may prevent the aberrant CP-AMPAR expression. Furthermore, recent molecular and pharmacological developments, particularly the discovery of TARP subtype-selective drugs, offer the exciting potential to modify some of the harmful effects of increased CP-AMPAR prevalence in a brain region-specific manner.

Indexed as

Neuronal PlasticityReceptors, AMPACalcium ChannelsNeuronsSynaptic TransmissionCalcium ChannelsReceptors, AMPAAMPA receptorsamyotrophic lateral sclerosisanoxiaauxiliary subunitscalcium-permeable AMPA receptorsCKAMP44cocainecornichonfear conditioningGluA2GSG1Lionotropic glutamate receptorsmalignant gliomaneurological disorderpainstargazinsynaptic plasticitysynaptic transmissionTARPs

Identifiers

PMID33533533
PMCPMC8436767
OpenAlexW3126330892

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.