Evidence map›Paper›PMID 25096398›Full record

ReviewCellular and molecular neurobiology2015

ATP signaling in brain: release, excitotoxicity and potential therapeutic targets.

Abraham Cisneros-Mejorado, Alberto Pérez-Samartín, Miroslav Gottlieb, Carlos Matute

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 90 citations in OpenAlex.

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  20. Diabetes and hypertension: Pivotal involvement of purinergic signaling.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
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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

4 authors at 3 institutions in 3 countries.

Abraham Cisneros-MejoradoAchucarro Basque Center for Neuroscience, Departamento de Neurociencias and CIBERNED, Universidad Del País Vasco, Leioa, Vizcaya, Spain.
Alberto Pérez-Samartín
Miroslav Gottlieb
Carlos Matute
Biomedical Research Networking Center on Neurodegenerative Diseases · ESAchucarro Basque Center for Neuroscience · ESInstitute of Neurobiology · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine 5'-triphosphate (ATP) is released as a genuine co-transmitter, or as a principal purinergic neurotransmitter, in an exocytotic and non-exocytotic manner. It activates ionotropic (P2X) and metabotropic (P2Y) receptors which mediate a plethora of functions in the brain. In particular, P2X7 receptor (P2X7R) are expressed in all brain cells and its activation can form a large pore allowing the passage of organic cations, the leakage of metabolites of up to 900 Da and the release of ATP itself. In turn, pannexins (Panx) are a family of proteins forming hemichannels that can release ATP. In this review, we summarize the progress in the understanding of the mechanisms of ATP release both in physiological and pathophysiological stages. We also provide data suggesting that P2X7R and pannexin 1 (Panx1) may form a large pore in cortical neurons as assessed by electrophysiology. Finally, the participation of calcium homeostasis modulator 1 is also suggested, another non-selective ion channel that can release ATP, and that could play a role in ischemic events, together with P2X7 and Panx1 during excitotoxicity by ATP.

Indexed as

Drug Delivery SystemsAdenosine TriphosphateAnimalsBrainHumansIon Channel GatingReceptors, Purinergic P2X7Adenosine TriphosphateReceptors, Purinergic P2X7

Identifiers

PMID25096398
PMCPMC11488175
OpenAlexW2069635085

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.