Evidence map›Paper›PMID 26852334›Full record

ArticleJournal of computational neuroscience2016

Large extracellular space leads to neuronal susceptibility to ischemic injury in a Na+/K+ pumps-dependent manner.

Niklas Hübel, R David Andrew, Ghanim Ullah

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Article in Journal of computational neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. On the origin of ultraslow spontaneous NaJournal of neurophysiology · 2021
    Article
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  8. 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

3 authors.

Niklas HübelDepartment of Physics, University of South Florida, Tampa, FL, 33620, USA. niklas.huebel@gmail.com.
R David AndrewDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Ghanim UllahDepartment of Physics, University of South Florida, Tampa, FL, 33620, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extent of anoxic depolarization (AD), the initial electrophysiological event during ischemia, determines the degree of brain region-specific neuronal damage. Neurons in higher brain regions exhibiting nonreversible, strong AD are more susceptible to ischemic injury as compared to cells in lower brain regions that exhibit reversible, weak AD. While the contrasting ADs in different brain regions in response to oxygen-glucose deprivation (OGD) is well established, the mechanism leading to such differences is not clear. Here we use computational modeling to elucidate the mechanism behind the brain region-specific recovery from AD. Our extended Hodgkin-Huxley (HH) framework consisting of neural spiking dynamics, processes of ion accumulation, and ion homeostatic mechanisms unveils that glial-vascular K(+) clearance and Na(+)/K(+)-exchange pumps are key to the cell's recovery from AD. Our phase space analysis reveals that the large extracellular space in the upper brain regions leads to impaired Na(+)/K(+)-exchange pumps so that they function at lower than normal capacity and are unable to bring the cell out of AD after oxygen and glucose is restored.

Indexed as

Models, NeurologicalAnimalsExtracellular SpaceGlucoseHumansHypoxiaIschemiaNeuronsNonlinear DynamicsSodium-Potassium-Exchanging ATPaseGlucoseSodium-Potassium-Exchanging ATPaseAnoxic depolarizationBrain injuryExtracellular volumeHodgkin–HuxleyIon dynamicsNeural mircoenvironment

Identifiers

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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.