Evidence map›Paper›PMID 24598811›Full record

ArticlePloS one2014

The nitric oxide donor SNAP-induced amino acid neurotransmitter release in cortical neurons. Effects of blockers of voltage-dependent sodium and calcium channels.

José Joaquín Merino, Carmen Arce, Ahmad Naddaf, Victor Bellver-Landete, Maria Jesús Oset-Gasque, María Pilar González

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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

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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 2 institutions in 2 countries.

José Joaquín MerinoDepartamento de Bioquímica y Biología Molecular II. Facultad de Farmacia, Universidad Complutense de Madrid (UCM), Madrid, Spain; Instituto Universitario de Investigación en Neuroquímica (IUIN). Universidad Complutense de Madrid (UCM), Madrid, Spain.
Carmen ArceDepartamento de Bioquímica y Biología Molecular II. Facultad de Farmacia, Universidad Complutense de Madrid (UCM), Madrid, Spain; Instituto Universitario de Investigación en Neuroquímica (IUIN). Universidad Complutense de Madrid (UCM), Madrid, Spain.
Ahmad NaddafFaculty of Pharmacy, Isra University, Amman, Jordan.
Victor Bellver-LandeteDepartamento de Bioquímica y Biología Molecular II. Facultad de Farmacia, Universidad Complutense de Madrid (UCM), Madrid, Spain; Instituto Universitario de Investigación en Neuroquímica (IUIN). Universidad Complutense de Madrid (UCM), Madrid, Spain.
Maria Jesús Oset-GasqueDepartamento de Bioquímica y Biología Molecular II. Facultad de Farmacia, Universidad Complutense de Madrid (UCM), Madrid, Spain; Instituto Universitario de Investigación en Neuroquímica (IUIN). Universidad Complutense de Madrid (UCM), Madrid, Spain.
María Pilar GonzálezDepartamento de Bioquímica y Biología Molecular II. Facultad de Farmacia, Universidad Complutense de Madrid (UCM), Madrid, Spain; Instituto Universitario de Investigación en Neuroquímica (IUIN). Universidad Complutense de Madrid (UCM), Madrid, Spain.
Universidad Complutense de Madrid · ESIsra University · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe discovery that nitric oxide (NO) functions as a signalling molecule in the nervous system has radically changed the concept of neuronal communication. NO induces the release of amino acid neurotransmitters but the underlying mechanisms remain to be elucidated.

findingsThe aim of this work was to study the effect of NO on amino acid neurotransmitter release (Asp, Glu, Gly and GABA) in cortical neurons as well as the mechanism underlying the release of these neurotransmitters. Cortical neurons were stimulated with SNAP, a NO donor, and the release of different amino acid neurotransmitters was measured by HPLC. The involvement of voltage dependent Na+ and Ca2+ channels as well as cGMP in its mechanism of action was evaluated.

conclusionsOur results indicate that NO induces release of aspartate, glutamate, glycine and GABA in cortical neurons and that this release is inhibited by ODQ, an inhibitor of soluble guanylate cyclase. Thus, the NO effect on amino acid neurotransmission could be mediated by cGMP formation in cortical neurons. Our data also demonstrate that the Na+ and Ca2+ voltage- dependent calcium channels are involved in the NO effects on cortical neurons.

Indexed as

Amino AcidsAnimalsBenzoatesCalcium Channel BlockersCalcium ChannelsCell SurvivalCerebral CortexFemaleGuanylate CyclaseImidazolesMembrane PotentialsModels, BiologicalNeuronsNeurotransmitter AgentsNitric Oxide DonorsOxadiazoles1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-oneAmino AcidsBenzoatesCalcium Channel BlockersCalcium ChannelsGuanylate CyclaseImidazolesNeurotransmitter AgentsNitric Oxide DonorsOxadiazolesQuinoxalinesReceptors, Cytoplasmic and NuclearS-Nitroso-N-AcetylpenicillamineSodium Channel BlockersSodium ChannelsSoluble Guanylyl Cyclase

Identifiers

PMID24598811
PMCPMC3944624
OpenAlexW2060808470

What OpenQuestion holds

Textmetadata
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.