Evidence map›Paper›PMID 17447081›Full record

ArticlePflugers Archiv : European journal of physiology2007

PIP(2)-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of PIP(2) depletion by Gq-coupled receptors in single living neurons.

Simon Hughes, Stephen J Marsh, Andrew Tinker, David A Brown

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Muscarinic Acetylcholine Receptors Modulate HCN Channel Properties in Vestibular Ganglion Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  2. Application of Fluorescent Proteins for Functional Dissection of theInternational journal of molecular sciences · 2021
    Review
  3. Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of physiology · 2017
    Article
  11. Fatty-acyl chain profiles of cellular phosphoinositides.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017
    Article
  12. Regulation of KCNQ/Kv7 family voltage-gated KBiochimica et biophysica acta. Biomembranes · 2017
    Review
  13. Article
  14. Modulation of Kv7 channels and excitability in the brain.Cellular and molecular life sciences : CMLS · 2017
    Review
  15. Article
  16. Activation of the CaPflugers Archiv : European journal of physiology · 2016
    Article
  17. Dynamics of Phosphoinositide-Dependent Signaling in Sympathetic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  18. Article
  19. Phosphoinositides regulate ion channels.Biochimica et biophysica acta · 2015
    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

4 authors at 1 institution in 1 country.

Simon HughesDepartment of Pharmacology, University College London, London, WC1E 6BT, UK.
Stephen J Marsh
Andrew Tinker
David A Brown
University College London · GB

Funding

British Heart FoundationMedical Research CouncilWellcome Trust
6 · The paper itself

Abstract

The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)P(2)). They can be closed on stimulating receptors that induce PI(4,5)P(2) hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)P(2), whereas closure by bradykinin B(2)-receptors (B2-BKRs) appears to result from formation of IP(3) and release of Ca(2+), implying that BKR stimulation does not deplete PI(4,5)P(2). We have used a fluorescently tagged PI(4,5)P(2)-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)P(2) changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)P(2) changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)P(2) was inhibited by wortmannin. Further, wortmannin 'rescued' M-current inhibition by BK after Ca(2+)-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)P(2) synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from Ca(2+) dependent to PI(4,5)P(2) dependent when PI(4,5)P(2) synthesis is inhibited.

Indexed as

Potassium Channel BlockersAnimalsBradykininCell MembraneCHO CellsCricetinaeCricetulusDNA, ComplementaryKCNQ2 Potassium ChannelMuscarinic AgonistsNeuronsPatch-Clamp TechniquesPhosphatidylinositol 4,5-DiphosphateRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledBradykininDNA, ComplementaryKCNQ2 Potassium ChannelMuscarinic AgonistsPhosphatidylinositol 4,5-DiphosphatePotassium Channel BlockersReceptors, G-Protein-CoupledReceptors, Muscarinic

Identifiers

PMID17447081
OpenAlexW2020173449

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.