Evidence map›Paper›PMID 23127996›Full record

ArticleMolecular and cellular neurosciences2013

Adar is essential for optimal presynaptic function.

Carolina Maldonado, Daniel Alicea, Maryvi Gonzalez, Maria Bykhovskaia, Bruno Marie

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.7field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. International journal of molecular sciences · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. RNA processing in neurological tissue: development, aging and disease.Seminars in cell & developmental biology · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. ADAR RNA editing below the backbone.RNA (New York, N.Y.) · 2017
    Review
  18. Article
  19. Cortactin Is a Regulator of Activity-Dependent Synaptic Plasticity Controlled by Wingless.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  20. 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

5 authors at 2 institutions in 1 country.

Carolina MaldonadoInstitute of Neurobiology, Medical Sciences Campus, University of Puerto Rico, PR.
Daniel Alicea
Maryvi Gonzalez
Maria Bykhovskaia
Bruno Marie
University of Puerto Rico, Medical Sciences Campus · PRCentral University of the Caribbean · PR

Funding

SUPPLEMENT FOR RENOVATION OF ANIMAL FACILITIES AT INSTITUTE OF NEUROBIOLOGYG12RR003051 · NCRR · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI ESPINO, ANA M · 1986 to 2011
$28.1M
Thyroid hormones and synaptic functionU54NS039408 · NINDS · UNIVERSIDAD CENTRAL DEL CARIBE · PI BYKHOVSKAIA, MARIA · 1999 to 2012
$14.0M
TRANSLATIONAL PROTEOMICS CENTERG12MD007600 · NIMHD · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI FERNANDEZ-REPOLLET, EMMA · 2012 to 2016
$11.0M
Encoding Long Term Stability of Neuronal FunctionSC2NS077924 · NINDS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI MARIE, BRUNO · 2011 to 2013
$445k
NCRR NIH HHS G12 RR003051NCRR NIH HHS RR-03051NIMHD NIH HHS G12 MD007600NINDS NIH HHS SC2 NS077924NINDS NIH HHS SC2NS077924NINDS NIH HHS U54 NS039408
6 · The paper itself

Abstract

RNA editing is a powerful way to recode genetic information. Because it potentially affects RNA targets that are predominantly present in neurons, it is widely hypothesized to affect neuronal structure and physiology. Across phyla, loss of the enzyme responsible for RNA editing, Adar, leads to behavioral changes, impaired locomotion, neurodegeneration and death. However, the consequences of a loss of Adar activity on neuronal structure and function have not been studied in detail. In particular, the role of RNA editing on synaptic development and physiology has not been investigated. Here we test the physiological and morphological consequences of the lack of Adar activity on the Drosophila neuromuscular junction (NMJ). Our detailed examination of synaptic transmission showed that loss of Adar increases quantal size, reduces the number of quanta of neurotransmitter released and perturbs the calcium dependence of synaptic release. In addition, we find that staining for several synaptic vesicle proteins is abnormally intense at Adar deficient synapses. Consistent with this finding, Adar mutants showed a major alteration in synaptic ultrastructure. Finally, we present evidence of compensatory changes in muscle membrane properties in response to the changes in presynaptic activity within the Adar mutant NMJs.

Indexed as

Adenosine DeaminaseAnimalsAnimals, Genetically ModifiedDrosophilaDrosophila ProteinsElectrophysiologyExocytosisImmunohistochemistryMicroscopy, Electron, TransmissionNeuromuscular JunctionNeurotransmitter AgentsRNA EditingSynapsesSynaptic TransmissionAdar protein, DrosophilaAdenosine DeaminaseDrosophila ProteinsNeurotransmitter Agents

Identifiers

PMID23127996
PMCPMC3613243
OpenAlexW2029818652

What OpenQuestion holds

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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.