Evidence map›Paper›PMID 12679375›Full record

ArticleThe Journal of physiology2003

Ecto-AMP deaminase blunts the ATP-derived adenosine A2A receptor facilitation of acetylcholine release at rat motor nerve endings.

M Teresa Magalhães-Cardoso, M Fátima Pereira, Laura Oliveira, J A Ribeiro, Rodrigo A Cunha, Paulo Correia-de-Sá

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2003. 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
1.6field-weighted citation impact, top 19% 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, 54 citations in OpenAlex.

  1. Trial
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  4. Feedback facilitation by adenosine APurinergic signalling · 2024
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  13. Isozymes of AMP-Deaminase in Muscles Myasthenia Gravis Patients.International journal of peptide research and therapeutics · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 3 institutions in 1 country.

M Teresa Magalhães-CardosoLaboratório de Farmacologia-UMIB, Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, Portugal.
M Fátima Pereira
Laura Oliveira
J A Ribeiro
Rodrigo A Cunha
Paulo Correia-de-Sá
Universidade do Porto · PTUniversity of Lisbon · PTUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At synapses, ATP is released and metabolised through ecto-nucleotidases forming adenosine, which modulates neurotransmitter release through inhibitory A1 or facilitatory A2A receptors, according to the amounts of extracellular adenosine. Neuromuscular junctions possess an ecto-AMP deaminase that can dissociate extracellular ATP catabolism from adenosine formation. In this study we have investigated the pattern of ATP release and its conversion into adenosine, to probe the role of ecto-AMP deaminase in controlling acetylcholine release from rat phrenic nerve terminals. Nerve-evoked ATP release was 28 +/- 12 pmol (mg tissue)-1 at 1 Hz, 54 +/- 3 pmol (mg tissue)-1 at 5 Hz and disproportionally higher at 50 Hz (324 +/- 23 pmol (mg tissue)-1). Extracellular ATP (30 microM) was metabolised with a half time of 8 +/- 2 min, being converted into ADP then into AMP. AMP was either dephosphorylated into adenosine by ecto-5'-nucleotidase (inhibited by ATP and blocked by 200 microM alpha,beta-methylene ADP) or deaminated into IMP by ecto-AMP deaminase (inhibited by 200 microM deoxycoformycin, which increased adenosine formation). Dephosphorylation and deamination pathways also catabolised endogenously released adenine nucleotides, since the nerve-evoked extracellular AMP accumulation was increased by either alpha,beta-methylene ADP (200 microM) or deoxycoformycin (200 microM). In the presence of nitrobenzylthioinosine (30 microM) to inhibit adenosine transport, deoxycoformycin (200 microM) facilitated nerve-evoked [3H]acetylcholine release by 77 +/- 9 %, an effect prevented by the A2A receptor antagonist, ZM 241385 (10 nM). It is concluded that, while ecto-5'-nucleotidase is inhibited by released ATP, ecto-AMP deaminase activity transiently blunts adenosine formation, which would otherwise reach levels high enough to activate facilitatory A2A receptors on motor nerve terminals.

Indexed as

AcetylcholineAdenosineAdenosine TriphosphateAMP DeaminaseAnimalsExtracellular FluidFemaleIn Vitro TechniquesMaleMotor NeuronsNerve EndingsRatsRats, WistarReceptor, Adenosine A2AAcetylcholineAdenosineAdenosine TriphosphateAMP DeaminaseEcto-AMP deaminase, ratReceptor, Adenosine A2A

Identifiers

PMID12679375
PMCPMC2342942
OpenAlexW2149253445

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.