Evidence map›Paper›PMID 32388797›Full record

ArticleMolecular neurobiology2020

Glial ATP and Large Pore Channels Modulate Synaptic Strength in Response to Chronic Inactivity.

Alberto Rafael, Andrea Cairus, Marina Tizzoni, Verónica Abudara, Nathalia Vitureira

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 16 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

5 authors at 1 institution in 1 country.

Alberto RafaelDepartamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
Andrea CairusDepartamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
Marina TizzoniDepartamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
Verónica AbudaraDepartamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
Nathalia VitureiraDepartamento de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay. nvitureira@fmed.edu.uy.ORCID https://orcid.org/0000-0003-1196-4094
Universidad de la República de Uruguay · UY

Funding

Comisión Sectorial de Investigación Científica 75
6 · The paper itself

Abstract

A key feature of neurotransmission is its ability to adapt to changes in neuronal environment, which is essential for many brain functions. Homeostatic synaptic plasticity (HSP) emerges as a compensatory mechanism used by neurons to adjust their excitability in response to changes in synaptic activity. Recently, glial cells emerged as modulators for neurotransmission by releasing gliotransmitters into the synaptic cleft through pathways that include P2X

Indexed as

Adenosine TriphosphateAnimalsConnexin 43ConnexinsHippocampusMiceMice, KnockoutNerve Tissue ProteinsNeurogliaNeuronsRatsReceptors, Purinergic P2X7SynapsesSynaptic TransmissionAdenosine TriphosphateConnexin 43ConnexinsNerve Tissue ProteinsPanx1 protein, mouseReceptors, Purinergic P2X7ATPCx43 hemichannelsHomeostatic synaptic plasticityNeuron-glia interactionPx1 channels

Identifiers

PMID32388797
OpenAlexW3021600524

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.