Evidence map›Paper›PMID 29590095›Full record

ArticlePLoS computational biology2018

Astrocytic Kir4.1 channels and gap junctions account for spontaneous epileptic seizure.

Mengmeng Du, Jiajia Li, Liang Chen, Yuguo Yu, Ying Wu

Abstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
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  13. The Anti-Epileptic Effects of Carbenoxolone In Vitro and In Vivo.International journal of molecular sciences · 2022
    Article
  14. Review
  15. Exacerbation of Epilepsy by Astrocyte Alkalization and Gap Junction Uncoupling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. Article
  17. Article
  18. Review
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.

Mengmeng DuState Key Laboratory for Strength and Vibration of Mechanical Structures, School of Aerospace, Xi'an Jiaotong University, Xi'an, China.
Jiajia LiState Key Laboratory for Strength and Vibration of Mechanical Structures, School of Aerospace, Xi'an Jiaotong University, Xi'an, China.
Liang ChenDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Yuguo YuState Key Laboratory of Medical Neurobiology, School of Life Science and Human Phenome Institute, Institutes of Brain Science, Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China.ORCID 0000-0003-0603-2890
Ying WuState Key Laboratory for Strength and Vibration of Mechanical Structures, School of Aerospace, Xi'an Jiaotong University, Xi'an, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental recordings in hippocampal slices indicate that astrocytic dysfunction may cause neuronal hyper-excitation or seizures. Considering that astrocytes play important roles in mediating local uptake and spatial buffering of K+ in the extracellular space of the cortical circuit, we constructed a novel model of an astrocyte-neuron network module consisting of a single compartment neuron and 4 surrounding connected astrocytes and including extracellular potassium dynamics. Next, we developed a new model function for the astrocyte gap junctions, connecting two astrocyte-neuron network modules. The function form and parameters of the gap junction were based on nonlinear regression fitting of a set of experimental data published in previous studies. Moreover, we have created numerical simulations using the above single astrocyte-neuron network module and the coupled astrocyte-neuron network modules. Our model validates previous experimental observations that both Kir4.1 channels and gap junctions play important roles in regulating the concentration of extracellular potassium. In addition, we also observe that changes in Kir4.1 channel conductance and gap junction strength induce spontaneous epileptic activity in the absence of external stimuli.

Indexed as

AnimalsAstrocytesComputational BiologyComputer SimulationEpilepsyGap JunctionsKcnj10 ChannelModels, NeurologicalPotassiumPotassium Channels, Inwardly RectifyingRatsSeizuresKcnj10 ChannelPotassiumPotassium Channels, Inwardly Rectifying

Identifiers

PMID29590095
PMCPMC5891073

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.