Evidence map›Paper›PMID 20305784›Full record

ArticlePloS one2010

Homer1a-dependent crosstalk between NMDA and metabotropic glutamate receptors in mouse neurons.

Federica Bertaso, Gautier Roussignol, Paul Worley, Joël Bockaert, Laurent Fagni, Fabrice Ango

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Spontaneous glutamate release activates mGluR signaling to drive rapid antidepressant responses.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  9. mGluR5 PAMs rescue cortical and behavioural defects in a mouse model of CDKL5 deficiency disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
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  19. Review
  20. The Effects of Antipsychotics on the Synaptic Plasticity GeneInternational journal of molecular sciences · 2020
    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

6 authors at 4 institutions in 2 countries.

Federica BertasoDepartement of Neurobiology, Institut de Génomique Fonctionnelle, CNRS UMR 5203, INSERM U661, Université de Montpellier 1 & 2, Montpellier, France.
Gautier Roussignol
Paul Worley
Joël Bockaert
Laurent Fagni
Fabrice Ango
Université de Montpellier · FRCentre National de la Recherche Scientifique · FRInstitut de Génomique Fonctionnelle · FRJohns Hopkins Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA large number of evidences suggest that group-I metabotropic glutamate receptors (mGluR1a, 1b, 1c, 5a, 5b) can modulate NMDA receptor activity. Interestingly, a physical link exists between these receptors through a Homer-Shank multi-protein scaffold that can be disrupted by the immediate early gene, Homer1a. Whether such a versatile link supports functional crosstalk between the receptors is unknown. METHODOLOGY/PRINCIPAL

findingsHere we used biochemical, electrophysiological and molecular biological approaches in cultured mouse cerebellar neurons to investigate this issue. We found that Homer1a or dominant negative Shank3 mutants that disrupt the physical link between the receptors allow inhibition of NMDA current by group-I mGluR agonist. This effect is antagonized by pertussis toxin, but not thapsigargin, suggesting the involvement of a G protein, but not intracellular calcium stores. Also, this effect is voltage-sensitive, being present at negative, but not positive membrane potentials. In the presence of DHPG, an apparent NMDA "tail current" was evoked by large pulse depolarization, only in neurons transfected with Homer1a. Co-immunoprecipitation experiments showed interaction between G-protein betagamma subunits and NMDA receptor in the presence of Homer1a and group-I mGluR agonist. CONCLUSIONS/SIGNIFICANCE: Altogether these results suggest a direct inhibition of NMDA receptor-channel by Gbetagamma subunits, following disruption of the Homer-Shank3 complex by the immediate early gene Homer1a. This study provides a new molecular mechanism by which group-I mGluRs could dynamically regulate NMDA receptor function.

Indexed as

Gene Expression RegulationAnimalsCalciumCarrier ProteinsElectrophysiologyGenes, DominantHomer Scaffolding ProteinsImmunoprecipitationMiceNeuronsN-MethylaspartatePatch-Clamp TechniquesReceptors, GlutamateReceptors, Metabotropic GlutamateCalciumCarrier ProteinsHomer Scaffolding ProteinsN-MethylaspartateReceptors, GlutamateReceptors, Metabotropic Glutamate

Identifiers

PMID20305784
PMCPMC2841198
OpenAlexW2020976619

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.