Evidence map›Paper›PMID 21723921›Full record

ArticleNeuroscience2011

Shaping of action potentials by type I and type II large-conductance Ca²+-activated K+ channels.

D B Jaffe, B Wang, R Brenner

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Review
  2. BK Channelopathies andAnnual review of physiology · 2024
    Review
  3. CaInternational journal of molecular sciences · 2023
    Review
  4. Article
  5. Anxiety and hippocampal neuronal activity: Relationship and potential mechanisms.Cognitive, affective & behavioral neuroscience · 2022
    Review
  6. Effect of an autism-associatedCurrent research in physiology · 2022
    Article
  7. Review
  8. Cell Type-Specific Decrease of the Intrinsic Excitability of Motor Cortical Pyramidal Neurons in Parkinsonism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  9. BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Journal of general physiology · 2019
    Review
  15. Article
  16. Review
  17. Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018
    Review
  18. Article
  19. Concise Whole-Cell Modeling of BKBiophysical journal · 2017
    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

3 authors.

D B JaffeDepartment of Biology, University of Texas at San Antonio, San Antonio, TX 78249, USA. david.jaffe@utsa.edu
B Wang
R Brenner

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

The BK channel is a Ca(2+) and voltage-gated conductance responsible for shaping action potential waveforms in many types of neurons. Type II BK channels are differentiated from type I channels by their pharmacology and slow gating kinetics. The β4 accessory subunit confers type II properties on BK α subunits. Empirically derived properties of BK channels, with and without the β4 accessory subunit, were obtained using a heterologous expression system under physiological ionic conditions. These data were then used to study how BK channels alone (type I) and with the accessory β4 subunit (type II) modulate action potential properties in biophysical neuron models. Overall, the models support the hypothesis that it is the slower kinetics provided by the β4 subunit that endows the BK channel with type II properties, which leads to broadening of action potentials and, secondarily, to greater recruitment of SK channels reducing neuronal excitability. Two regions of parameter space distinguished type II and type I effects; one where the range of BK-activating Ca(2+) was high (>20 μM) and the other where BK-activating Ca(2+) was low (∼0.4-1.2 μM). The latter required an elevated BK channel density, possibly beyond a likely physiological range. BK-mediated sharpening of the spike waveform associated with the lack of the β4 subunit was sensitive to the properties of voltage-gated Ca(2+) channels due to electrogenic effects on spike duration. We also found that depending on Ca(2+) dynamics, type II BK channels may have the ability to contribute to the medium AHP, a property not generally ascribed to BK channels, influencing the frequency-current relationship. Finally, we show how the broadening of action potentials conferred by type II BK channels can also indirectly increase the recruitment of SK-type channels decreasing the excitability of the neuron.

Indexed as

Models, NeurologicalAction PotentialsAnimalsComputer SimulationHEK293 CellsHumansIon Channel GatingLarge-Conductance Calcium-Activated Potassium ChannelsMicePatch-Clamp TechniquesLarge-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID21723921
PMCPMC3166373

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.