Evidence map›Paper›PMID 20534576›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

The KCNQ5 potassium channel mediates a component of the afterhyperpolarization current in mouse hippocampus.

Anastassios V Tzingounis, Matthias Heidenreich, Tatjana Kharkovets, Guillermo Spitzmaul, Henrik S Jensen, Roger A Nicoll, Thomas J Jentsch

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. KArchiv der Pharmazie · 2026
    Review
  3. Article
  4. Phosphatidylinositol 4,5-bisphosphate activation mechanism of human KCNQ5.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. Cholinergic regulation of dendritic CaProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Polymodal KCommunications biology · 2024
    Article
  13. KAddiction biology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. HumanJournal of neurophysiology · 2022
    Article
  20. Article

22 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 3 countries.

Anastassios V TzingounisDepartment of Cellular and Molecular Pharmacology and Department of Physiology, University of California, San Francisco, CA 94143, USA.
Matthias Heidenreich
Tatjana Kharkovets
Guillermo Spitzmaul
Henrik S Jensen
Roger A Nicoll
Thomas J Jentsch
Leibniz-Forschungsinstitut für Molekulare Pharmakologie · DEUniversität Hamburg · DEUniversity of California, San Francisco · USUniversity of Copenhagen · DK

Funding

NEUROTRANSMITTER EFFECTS ON LOCAL NEURONAL CIRCUITSR37MH038256 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 1987 to 2016
$9.0M
Molecular components of the calcium activated slow afterhyperpolarizationK99NS060890 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TZINGOUNIS, ANASTASIOS · 2008 to 2008
$79k
NIMH NIH HHS R37 MH038256NINDS NIH HHS K99 NS060890
6 · The paper itself

Abstract

Mutations in KCNQ2 and KCNQ3 voltage-gated potassium channels lead to neonatal epilepsy as a consequence of their key role in regulating neuronal excitability. Previous studies in the brain have focused primarily on these KCNQ family members, which contribute to M-currents and afterhyperpolarization conductances in multiple brain areas. In contrast, the function of KCNQ5 (Kv7.5), which also displays widespread expression in the brain, is entirely unknown. Here, we developed mice that carry a dominant negative mutation in the KCNQ5 pore to probe whether it has a similar function as other KCNQ channels. This mutation renders KCNQ5(dn)-containing homomeric and heteromeric channels nonfunctional. We find that Kcnq5(dn/dn) mice are viable and have normal brain morphology. Furthermore, expression and neuronal localization of KCNQ2 and KCNQ3 subunits are unchanged. However, in the CA3 area of hippocampus, a region that highly expresses KCNQ5 channels, the medium and slow afterhyperpolarization currents are significantly reduced. In contrast, neither current is affected in the CA1 area of the hippocampus, a region with low KCNQ5 expression. Our results demonstrate that KCNQ5 channels contribute to the afterhyperpolarization currents in hippocampus in a cell type-specific manner.

Indexed as

Amino Acid SubstitutionAnimalsBase SequenceDNAFemaleGene Knock-In TechniquesHippocampusIn Vitro TechniquesKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelKCNQ Potassium ChannelsMembrane PotentialsMiceMice, Mutant StrainsMice, TransgenicMolecular Sequence DataDNAKCNQ2 Potassium ChannelKcnq2 protein, mouseKCNQ3 Potassium ChannelKcnq3 protein, mouseKCNQ5 channel, mouseKCNQ Potassium ChannelsMutant ProteinsNerve Tissue Proteins

Identifiers

PMID20534576
PMCPMC2890451
OpenAlexW2025801454

What OpenQuestion holds

Textmetadata
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.