Evidence map›Paper›PMID 24367293›Full record

ArticleFrontiers in cellular neuroscience2013

Regulation of action potential delays via voltage-gated potassium Kv1.1 channels in dentate granule cells during hippocampal epilepsy.

Florian Kirchheim, Stefanie Tinnes, Carola A Haas, Michael Stegen, Jakob Wolfart

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Neural excitability increases with axonal resistance between soma and axon initial segment.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. KScientific reports · 2021
    Article
  9. Article
  10. Homeostatic Plasticity in Epilepsy.Frontiers in cellular neuroscience · 2020
    Article
  11. Article
  12. Review
  13. Constitutive and Synaptic Activation of GIRK Channels Differentiates Mature and Newborn Dentate Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  14. Article
  15. Article
  16. Position- and Time-DependentFrontiers in cellular neuroscience · 2018
    Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 2 institutions in 2 countries.

Florian KirchheimCellular Neurophysiology, Department of Neurosurgery, University Medical Center Freiburg Freiburg, Germany ; Faculty of Biology, University of Freiburg Freiburg, Germany.
Stefanie TinnesExperimental Epilepsy Research, Department of Neurosurgery, University Medical Center Freiburg Freiburg, Germany.
Carola A HaasExperimental Epilepsy Research, Department of Neurosurgery, University Medical Center Freiburg Freiburg, Germany.
Michael StegenCellular Neurophysiology, Department of Neurosurgery, University Medical Center Freiburg Freiburg, Germany ; Department of Biomedicine, Institute of Physiology, University of Basel Basel, Switzerland.
Jakob WolfartCellular Neurophysiology, Department of Neurosurgery, University Medical Center Freiburg Freiburg, Germany ; Oscar Langendorff Institute of Physiology, University of Rostock Rostock, Germany.
University Medical Center Freiburg · DEUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Action potential (AP) responses of dentate gyrus granule (DG) cells have to be tightly regulated to maintain hippocampal function. However, which ion channels control the response delay of DG cells is not known. In some neuron types, spike latency is influenced by a dendrotoxin (DTX)-sensitive delay current (ID) mediated by unidentified combinations of voltage-gated K(+) (Kv) channels of the Kv1 family Kv1.1-6. In DG cells, the ID has not been characterized and its molecular basis is unknown. The response phenotype of mature DG cells is usually considered homogenous but intrinsic plasticity likely occurs in particular in conditions of hyperexcitability, for example during temporal lobe epilepsy (TLE). In this study, we examined response delays of DG cells and underlying ion channel molecules by employing a combination of gramicidin-perforated patch-clamp recordings in acute brain slices and single-cell reverse transcriptase quantitative polymerase chain reaction (SC RT-qPCR) experiments. An in vivo mouse model of TLE consisting of intrahippocampal kainate (KA) injection was used to examine epilepsy-related plasticity. Response delays of DG cells were DTX-sensitive and strongly increased in KA-injected hippocampi; Kv1.1 mRNA was elevated 10-fold, and the response delays correlated with Kv1.1 mRNA abundance on the single cell level. Other Kv1 subunits did not show overt changes in mRNA levels. Kv1.1 immunolabeling was enhanced in KA DG cells. The biophysical properties of ID and a delay heterogeneity within the DG cell population was characterized. Using organotypic hippocampal slice cultures (OHCs), where KA incubation also induced ID upregulation, the homeostatic reversibility and neuroprotective potential for DG cells were tested. In summary, the AP timing of DG cells is effectively controlled via scaling of Kv1.1 subunit transcription. With this antiepileptic mechanism, DG cells delay their responses during hyperexcitation.

Indexed as

hippocampushomeostasishomeostatic plasticityKcna1KDshaker-related

Identifiers

PMID24367293
PMCPMC3852106
OpenAlexW1979339760

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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.