Evidence map›Paper›PMID 30132892›Full record

ArticleThe Journal of physiology2018

Inhibition of GluN2A NMDA receptors ameliorates synaptic plasticity deficits in the Fmr1

Camilla J Lundbye, Anna Karina H Toft, Tue G Banke

Open access · goldAbstract read
In one paragraph

Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  8. Current neuropharmacology · 2025
    Review
  9. Article
  10. GluN2A: A Promising Target for Developing Novel Antidepressants.The international journal of neuropsychopharmacology · 2024
    Review
  11. Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  12. Article
  13. Article
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  15. Article
  16. Review
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  18. Article
  19. Synaptopathology Involved in Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2018
    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

3 authors at 1 institution in 1 country.

Camilla J LundbyeInstitute of Biomedicine - Physiology, Aarhus University, DK-8000, Aarhus, Denmark.
Anna Karina H ToftInstitute of Biomedicine - Physiology, Aarhus University, DK-8000, Aarhus, Denmark.
Tue G BankeInstitute of Biomedicine - Physiology, Aarhus University, DK-8000, Aarhus, Denmark.ORCID 0000-0001-8417-4400
Aarhus University · DK

Funding

Det Frie Forskningsråd (Danish Council for Independent Research) DFF - 4004-00188Lundbeckfonden (Lundbeck Foundation) 2011-8826Riisfort
6 · The paper itself

Abstract

key pointsFragile X syndrome (FXS) is a genetic condition that is the most common form of inherited intellectual impairment and causes a range of neurodevelopmental complications including learning disabilities and intellectual disability and shares many characteristics with autism spectrum disorder (ASD). In the FXS mouse model, Fmr1 ABSTRACT: NMDA receptors (NMDARs) play important roles in synaptic plasticity at central excitatory synapses, and dysregulation of their function may lead to severe disorders such Fragile X syndrome (FXS). FXS is caused by transcriptional silencing of the FMR1 gene followed by lack of the encoding protein. Here we examined the effects of pharmacological and genetic manipulation of hippocampal NMDAR functions in long-term potentiation (LTP) and depression (LTD). We found impaired NMDAR-dependent LTP in the Fmr1-deficient mice, which could be fully restored when GluN2A-containing NMDARs was pharmacological inhibited. Interestingly, similar LTP effects were observed when the GluN2A gene (Grin2a) was deleted in Fmr1

Indexed as

Neuronal PlasticityAnimalsCA1 Region, HippocampalExcitatory Amino Acid AntagonistsFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeMaleMiceMice, Inbred C57BLReceptors, N-Methyl-D-AspartateExcitatory Amino Acid AntagonistsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Receptors, N-Methyl-D-AspartateAutismDevelopmental DisabilityFragile X syndromeGluN2AGlutamate receptorsIntellectual Disabilityneuropsychiatric diseasesSynaptic plasticitytri-heteromeric NMDA receptors

Identifiers

PMID30132892
PMCPMC6187029
OpenAlexW2891108904

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.