Evidence map›Paper›PMID 25625181›Full record

ArticleRNA biology2015

Chronic glutamate treatment selectively modulates AMPA RNA editing and ADAR expression and activity in primary cortical neurons.

Daniela Bonini, Alice Filippini, Luca La Via, Chiara Fiorentini, Fabio Fumagalli, Marina Colombi, Alessandro Barbon

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Explaining Pathogenicity of Congenital Zika and Guillain-Barré Syndromes: Does Dysregulation of RNA Editing Play a Role?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019
    Article
  12. Review
  13. Review
  14. 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

7 authors at 4 institutions in 3 countries.

Daniela Boninia Biology and Genetic Division; Department of Molecular and Translational Medicine; National Institute of Neuroscience; University of Brescia ; Brescia , Italy.
Alice Filippini
Luca La Via
Chiara Fiorentini
Fabio Fumagalli
Marina Colombi
Alessandro Barbon
University of Brescia · ITNational Neuroscience Institute · SGBrescia University · USUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine-to-inosine RNA editing is a post-transcriptional process, catalyzed by ADAR enzymes, with an important role in diversifying the number of proteins derived from a single gene. In neurons, editing of ionotropic AMPA glutamate receptors has been shown to be altered under several experimental conditions, including severe pathologies, thus highlighting the potential significance of its modulation. In this study, we treated rat primary cortical cell cultures with a sub-lethal dose of glutamate (10 μM), focusing on RNA editing and ADAR activity. We found that chronic glutamate treatment down-regulates RNA editing levels at the R/G site of GluA2-4 subunits of AMPA receptors and at the K/E site of CYFIP2. These changes are site-specific since they were not observed either for the GluA2 Q/R site or for other non-glutamatergic sites. Glutamate treatment also down-regulates the protein expression levels of both ADAR1 and ADAR2 enzymes, through a pathway that is Ca(2+)- and calpain-dependent. Given that AMPA receptors containing unedited subunits show a slower recovery rate from desensitization compared to those containing edited forms, the reduced editing at the R/G site may, at least in part, compensate for glutamate over-stimulation, perhaps through the reduced activation of postsynaptic receptors. In summary, our data provide direct evidence of the involvement of ADAR1 and ADAR2 activity as a possible compensatory mechanism for neuronal protection following glutamate over-stimulation.

Indexed as

Adenosine DeaminaseAnimalsCalciumCalpainCell LineCell SurvivalGlutamic AcidMembrane ProteinsNeuronsPrimary Cell CultureRats, Sprague-DawleyReceptors, AMPARNA, MessengerAda protein, ratADAR1 protein, ratAdarb1 protein, ratAdenosine DeaminaseCalciumCalpainGlutamic AcidMembrane ProteinsReceptors, AMPARNA, MessengerADAR1ADAR2AMPA receptorsglutamate treatmentR/G siteRNA editing

Identifiers

PMID25625181
PMCPMC4615659
OpenAlexW1780209601

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.