Evidence map›Paper›PMID 26136660›Full record

ArticleFrontiers in cellular neuroscience2015

Disruption of Slc4a10 augments neuronal excitability and modulates synaptic short-term plasticity.

Anne Sinning, Lutz Liebmann, Christian A Hübner

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. The role of NaPflugers Archiv : European journal of physiology · 2024
    Review
  7. Article
  8. Potential Theranostic Roles of SLC4 Molecules in Human Diseases.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The therapeutic importance of acid-base balance.Biochemical pharmacology · 2021
    Review
  14. Article
  15. Article
  16. Early Hearing Loss upon Disruption of Slc4a10 in C57BL/6 Mice.Journal of the Association for Research in Otolaryngology : JARO · 2019
    Article
  17. Article
  18. Article
  19. Mouse models of SLC4-linked disorders of HCOAmerican journal of physiology. Cell physiology · 2018
    Review
  20. Article
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 at 2 institutions in 1 country.

Anne SinningInstitute of Human Genetics, University Hospital Jena, Friedrich Schiller University Jena Jena, Germany ; Institute of Physiology, University Medical Center of the Johannes Gutenberg University Mainz, Germany.
Lutz LiebmannInstitute of Human Genetics, University Hospital Jena, Friedrich Schiller University Jena Jena, Germany.
Christian A HübnerInstitute of Human Genetics, University Hospital Jena, Friedrich Schiller University Jena Jena, Germany.
Friedrich Schiller University Jena · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Slc4a10 is a Na(+)-coupled Cl(-)-HCO3 (-) exchanger, which is expressed in principal and inhibitory neurons as well as in choroid plexus epithelial cells of the brain. Slc4a10 knockout (KO) mice have collapsed brain ventricles and display an increased seizure threshold, while heterozygous deletions in man have been associated with idiopathic epilepsy and other neurological symptoms. To further characterize the role of Slc4a10 for network excitability, we compared input-output relations as well as short and long term changes of evoked field potentials in Slc4a10 KO and wildtype (WT) mice. While responses of CA1 pyramidal neurons to stimulation of Schaffer collaterals were increased in Slc4a10 KO mice, evoked field potentials did not differ between genotypes in the stratum radiatum or the neocortical areas analyzed. Paired pulse facilitation was diminished in the hippocampus upon disruption of Slc4a10. In the neocortex paired pulse depression was increased. Though short term plasticity is modulated via Slc4a10, long term potentiation appears independent of Slc4a10. Our data support that Slc4a10 dampens neuronal excitability and thus sheds light on the pathophysiology of SLC4A10 associated pathologies.

Indexed as

field potentialGABAergic inhibitionLTPSlc4a10synaptic plasticity

Identifiers

PMID26136660
PMCPMC4468864
OpenAlexW1547480653

What OpenQuestion holds

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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.