Evidence map›Paper›PMID 21848922›Full record

ArticleThe European journal of neuroscience2011

Modulation by the BK accessory β4 subunit of phosphorylation-dependent changes in excitability of dentate gyrus granule neurons.

David Petrik, Bin Wang, Robert Brenner

Abstract read
In one paragraph

Article in The European journal of neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. CaInternational journal of molecular sciences · 2023
    Review
  2. Article
  3. Article
  4. Mechanism of Manganese Dysregulation of Dopamine Neuronal Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  5. The Journal of general physiology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Methamphetamine Regulation of Firing Activity of Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  11. BK Channels in the Central Nervous System.International review of neurobiology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

David PetrikDepartment of Physiology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Bin Wang
Robert Brenner
The University of Texas Health Science Center at San Antonio · US

Funding

BK Channel B4 Subunit in the Dentate Gyrus and SeizuresR01NS052574 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BRENNER, ROBERT · 2007 to 2011
$1.3M
NINDS NIH HHS NS052574NINDS NIH HHS R01 NS052574
6 · The paper itself

Abstract

Large-conductance voltage- and calcium-activated potassium (BK) channels are large-conductance calcium- and voltage-activated potassium channels critical for neuronal excitability. Some neurons express so called fast-gated, type I BK channels. Other neurons express BK channels assembled with the accessory β4 subunit conferring slow gating of type II BK channels. However, it is not clear how protein phosphorylation modulates these two distinct BK channel types. Using β4-knockout mice, we compared fast- or slow-gated BK channels in response to changes in phosphorylation status of hippocampus dentate gyrus granule neurons. We utilized the selective PP2A/PP4 phosphatase inhibitor Fostriecin to study changes in action potential shape and firing properties of the neurons. In β4-knockout neurons, Fostriecin increases BK current, speeds up BK channel activation and reduces action potential amplitudes. Fostriecin increases spiking during early components of an action potential train. In contrast, inhibition of BK channels through β4 in wild-type neurons or by the BK channel inhibitor Paxilline opposes Fostriecin effects. Voltage clamp recordings of neurons reveal that Fostriecin increases both calcium and BK currents. However, Fostriecin does not activate BK α channels in transfected HEK293 cells lacking calcium channels. In summary, these results suggest that fast-gating, type I BK channels lacking β4 can increase neuronal excitability in response to reduced phosphatase activity and activation of calcium channels. By opposing BK channel activation, the β4 subunit plays an important role in moderating firing frequency regardless of changes in phosphorylation status.

Indexed as

Action PotentialsAnimalsCyclic AMPDentate GyrusEnzyme InhibitorsHEK293 CellsHumansLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsMiceMice, Inbred C57BLMice, KnockoutNeuronsPatch-Clamp TechniquesPhosphoprotein PhosphatasesPhosphorylationPolyenesCyclic AMPEnzyme InhibitorsfostriecinLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsPhosphoprotein PhosphatasesPolyenesProtein Phosphatase 2protein phosphatase 4Pyrones

Identifiers

PMID21848922
PMCPMC3168689
OpenAlexW1576836351

What OpenQuestion holds

Textmetadata
LicenceTDM
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.