Evidence map›Paper›PMID 19103683›Full record

ArticleThe Journal of physiology2009

Synaptic ionotropic glutamate receptors and plasticity are developmentally altered in the CA1 field of Fmr1 knockout mice.

Yair Pilpel, Aleksander Kolleker, Sven Berberich, Melanie Ginger, Andreas Frick, Edwin Mientjes, Ben A Oostra, Peter H Seeburg

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. GABAergic Progenitor Cell Graft Rescues Cognitive Deficits in Fragile X Syndrome Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. 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
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. New Therapeutic Options for Fragile X Syndrome.Current treatment options in neurology · 2019
    Review
  14. Review
  15. Article
  16. ASD-AssociatedFrontiers in cellular neuroscience · 2018
    Article
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Yair PilpelMax Planck Institute for Medical Research, Department of Molecular Neurobiology, Heidelberg, Germany. yair.pilpel@mpimf-heidelberg.mpg.de
Aleksander Kolleker
Sven Berberich
Melanie Ginger
Andreas Frick
Edwin Mientjes
Ben A Oostra
Peter H Seeburg
Max Planck Institute for Medical Research · DEErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fragile X syndrome is one of the most common forms of mental retardation, yet little is known about the physiological mechanisms causing the disease. In this study, we probed the ionotropic glutamate receptor content in synapses of hippocampal CA1 pyramidal neurons in a mouse model for fragile X (Fmr1 KO2). We found that Fmr1 KO2 mice display a significantly lower AMPA to NMDA ratio than wild-type mice at 2 weeks of postnatal development but not at 6-7 weeks of age. This ratio difference at 2 weeks postnatally is caused by down-regulation of the AMPA and up-regulation of the NMDA receptor components. In correlation with these changes, the induction of NMDA receptor-dependent long-term potentiation following a low-frequency pairing protocol is increased in Fmr1 KO2 mice at this developmental stage but not later in maturation. We propose that ionotropic glutamate receptors, as well as potentiation, are altered at a critical time point for hippocampal network development, causing long-term changes. Associated learning and memory deficits would contribute to the fragile X mental retardation phenotype.

Indexed as

AnimalsAnimals, NewbornFragile X Messenger Ribonucleoprotein 1Gene Expression Regulation, DevelopmentalHippocampusLong-Term PotentiationMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityReceptors, AMPAReceptors, GlutamateReceptors, N-Methyl-D-AspartateSynapsesFragile X Messenger Ribonucleoprotein 1Receptors, AMPAReceptors, GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID19103683
PMCPMC2669971
OpenAlexW2168156908

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.