Evidence map›Paper›PMID 25093813›Full record

ArticlePloS one2014

Adenosine A2A receptors activation facilitates neuromuscular transmission in the pre-symptomatic phase of the SOD1(G93A) ALS mice, but not in the symptomatic phase.

Filipe Nascimento, Paula A Pousinha, Alexandra M Correia, Rui Gomes, Ana M Sebastião, Joaquim A Ribeiro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
2.4field-weighted citation impact, top 13% 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, 39 citations in OpenAlex.

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  16. Opposite Synaptic Alterations at the Neuromuscular Junction in an ALS Mouse Model: When Motor Units Matter.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  17. Review
  18. Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017
    Review
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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 1 institution in 1 country.

Filipe NascimentoInstitute of Pharmacology and Neurosciences, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Unit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal.
Paula A PousinhaInstitute of Pharmacology and Neurosciences, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Unit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal.
Alexandra M CorreiaUnit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal; National Museum of Natural History and Science, University of Lisbon, Lisbon, Portugal.
Rui GomesUnit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal; Faculty of Sciences, University of Lisbon, Lisbon, Portugal.
Ana M SebastiãoInstitute of Pharmacology and Neurosciences, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Unit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal.
Joaquim A RibeiroInstitute of Pharmacology and Neurosciences, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Unit of Neurosciences, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal.
University of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease leading to motor neuron dysfunction resulting in impairment of neuromuscular transmission. A2A adenosine receptors have already been considered as a potential therapeutical target for ALS but their neuromodulatory role at the neuromuscular junction in ALS remains to be clarified. In the present work, we evaluated the effects of A2A receptors on neuromuscular transmission of an animal model of ALS: SOD1(G93A) mice either in the pre-symptomatic (4-6 weeks old) or in the symptomatic (12-14 weeks old) stage. Electrophysiological experiments were performed obtaining intracellular recordings in Mg2+ paralyzed phrenic nerve-hemidiaphragm preparations. Endplate potentials (EPPs), quantal content (q. c.) of EPPs, miniature endplate potentials (MEPPs) and giant miniature endplate potential (GMEPPs) were recorded. In the pre-symptomatic phase of the disease (4-6 weeks old mice), the selective A2A receptor agonist, CGS 21680, significantly enhanced (p<0.05 Unpaired t-test) the mean amplitude and q.c. of EPPs, and the frequency of MEPPs and GMEPPs at SOD1(G93A) neuromuscular junctions, the effect being of higher magnitude (p<0.05, Unpaired t-test) than age-matched control littermates. On the contrary, in symptomatic mice (12-14 weeks old), CGS 21680 was devoid of effect on both the amplitude and q.c. of EPPs and the frequency of MEPPs and GMEPPs (p<0.05 Paired t-test). The results herein reported clearly document that at the neuromuscular junction of SOD1(G93A) mice there is an exacerbation of A2A receptor-mediated excitatory effects at the pre-symptomatic phase, whereas in the symptomatic phase A2A receptor activation is absent. The results thus suggest that A2A receptors function changes with ALS progression.

Indexed as

Synaptic TransmissionAdenosineAmyotrophic Lateral SclerosisAnimalsDisease ProgressionExcitatory Postsynaptic PotentialsHumansMaleMice, TransgenicMotor EndplateMutationNeuromuscular JunctionPhenethylaminesReceptor, Adenosine A2ASuperoxide Dismutase2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosineAdenosinePhenethylaminesReceptor, Adenosine A2ASuperoxide Dismutase

Identifiers

PMID25093813
PMCPMC4122437
OpenAlexW1981149039

What OpenQuestion holds

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LicenceCC BY
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.