Evidence map›Paper›PMID 26009774›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015

Glial cell regulation of neuronal activity and blood flow in the retina by release of gliotransmitters.

Eric A Newman

Open access · bronzeAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
11.9field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 192 citations in OpenAlex.

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  15. Cells · 2024
    Review
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  20. Age-Related Macular Degeneration, a Mathematically Tractable Disease.Investigative ophthalmology & visual science · 2024
    Review

55 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Eric A NewmanDepartment of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street SE, Minneapolis, MN 55455, USA ean@umn.edu.
University of Minnesota · US

Funding

Visual TestingP30EY011374 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NEWMAN, ERIC A · 1996 to 2019
$8.8M
PHYSIOLOGY OF RETINAL MULLER CELLS AND ASTROCYTESR01EY004077 · NEI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI NEWMAN, ERIC A · 1985 to 2013
$5.7M
Dark adaptation and hypoxia in diabetic retinopathyR21EY023216 · NEI · UNIVERSITY OF MINNESOTA · PI NEWMAN, ERIC A · 2013 to 2014
$414k
NEI NIH HHS P30 EY011374NEI NIH HHS P30-EY11374NEI NIH HHS R01 EY004077NEI NIH HHS R21 EY023216
6 · The paper itself

Abstract

Astrocytes in the brain release transmitters that actively modulate neuronal excitability and synaptic efficacy. Astrocytes also release vasoactive agents that contribute to neurovascular coupling. As reviewed in this article, Müller cells, the principal retinal glial cells, modulate neuronal activity and blood flow in the retina. Stimulated Müller cells release ATP which, following its conversion to adenosine by ectoenzymes, hyperpolarizes retinal ganglion cells by activation of A1 adenosine receptors. This results in the opening of G protein-coupled inwardly rectifying potassium (GIRK) channels and small conductance Ca(2+)-activated K(+) (SK) channels. Tonic release of ATP also contributes to the generation of tone in the retinal vasculature by activation of P2X receptors on vascular smooth muscle cells. Vascular tone is lost when glial cells are poisoned with the gliotoxin fluorocitrate. The glial release of vasoactive metabolites of arachidonic acid, including prostaglandin E2 (PGE2) and epoxyeicosatrienoic acids (EETs), contributes to neurovascular coupling in the retina. Neurovascular coupling is reduced when neuronal stimulation of glial cells is interrupted and when the synthesis of arachidonic acid metabolites is blocked. Neurovascular coupling is compromised in diabetic retinopathy owing to the loss of glial-mediated vasodilation. This loss can be reversed by inhibiting inducible nitric oxide synthase. It is likely that future research will reveal additional important functions of the release of transmitters from glial cells.

Indexed as

Action PotentialsEpendymoglial CellsG Protein-Coupled Inwardly-Rectifying Potassium ChannelsHumansNeurotransmitter AgentsRegional Blood FlowRetinal NeuronsRetinal VesselsSmall-Conductance Calcium-Activated Potassium ChannelsG Protein-Coupled Inwardly-Rectifying Potassium ChannelsNeurotransmitter AgentsSmall-Conductance Calcium-Activated Potassium Channelsastrocyteblood flowdiabetic retinopathygliotransmittersneurovascular couplingretina

Identifiers

PMID26009774
PMCPMC4455764
OpenAlexW2230531921

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.