Evidence map›Paper›PMID 29659572›Full record

ArticlePLoS computational biology2018

A computational study of astrocytic glutamate influence on post-synaptic neuronal excitability.

Bronac Flanagan, Liam McDaid, John Wade, KongFatt Wong-Lin, Jim Harkin

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Astrocytic modulation of neuronal signalling.Frontiers in network physiology · 2023
    Review
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  16. Serum NMR metabolomics uncovers multiple metabolic changes in phenobarbital-treated dogs.Metabolomics : Official journal of the Metabolomic Society · 2021
    Article
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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.

Bronac FlanaganIntelligent Systems Research Centre, University of Ulster, Magee Campus, Derry~Londonderry, Northern Ireland, United Kingdom.ORCID 0000-0002-9697-7478
Liam McDaidIntelligent Systems Research Centre, University of Ulster, Magee Campus, Derry~Londonderry, Northern Ireland, United Kingdom.
John WadeIntelligent Systems Research Centre, University of Ulster, Magee Campus, Derry~Londonderry, Northern Ireland, United Kingdom.ORCID 0000-0003-1300-9429
KongFatt Wong-LinIntelligent Systems Research Centre, University of Ulster, Magee Campus, Derry~Londonderry, Northern Ireland, United Kingdom.
Jim HarkinIntelligent Systems Research Centre, University of Ulster, Magee Campus, Derry~Londonderry, Northern Ireland, United Kingdom.
University of Ulster · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of astrocytes to rapidly clear synaptic glutamate and purposefully release the excitatory transmitter is critical in the functioning of synapses and neuronal circuits. Dysfunctions of these homeostatic functions have been implicated in the pathology of brain disorders such as mesial temporal lobe epilepsy. However, the reasons for these dysfunctions are not clear from experimental data and computational models have been developed to provide further understanding of the implications of glutamate clearance from the extracellular space, as a result of EAAT2 downregulation: although they only partially account for the glutamate clearance process. In this work, we develop an explicit model of the astrocytic glutamate transporters, providing a more complete description of the glutamate chemical potential across the astrocytic membrane and its contribution to glutamate transporter driving force based on thermodynamic principles and experimental data. Analysis of our model demonstrates that increased astrocytic glutamate content due to glutamine synthetase downregulation also results in increased postsynaptic quantal size due to gliotransmission. Moreover, the proposed model demonstrates that increased astrocytic glutamate could prolong the time course of glutamate in the synaptic cleft and enhances astrocyte-induced slow inward currents, causing a disruption to the clarity of synaptic signalling and the occurrence of intervals of higher frequency postsynaptic firing. Overall, our work distilled the necessity of a low astrocytic glutamate concentration for reliable synaptic transmission of information and the possible implications of enhanced glutamate levels as in epilepsy.

Indexed as

Models, NeurologicalAnimalsAstrocytesCalcium SignalingComputational BiologyComputer SimulationExcitatory Amino Acid Transporter 2Excitatory Postsynaptic PotentialsGlutamic AcidHumansNeural PathwaysNeuronsSynapsesSynaptic TransmissionExcitatory Amino Acid Transporter 2Glutamic Acid

Identifiers

PMID29659572
PMCPMC5919689
OpenAlexW2799844935

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.