Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Does diacylglycerol regulate KCNQ channels?

Byung-Chang Suh1, Bertil Hille

  • 1Department of Physiology and Biophysics, University of Washington School of Medicine, G-424 Health Sciences Building, P.O. Box 357290, Seattle, WA, 98195-7290, USA.

Pflugers Archiv : European Journal of Physiology
|May 25, 2006
PubMed
Summary

Diacylglycerols do not regulate KCNQ2/KCNQ3 channels. Muscarinic receptor activation does not involve diacylglycerols in KCNQ channel regulation, even when phospholipase C is activated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

TWIK-1 plays distinct roles in spinal and peripheral sensory circuits controlling mechanical sensitivity and neuropathic hypersensitivity.

Signal transduction and targeted therapy·2026
Same author

TMEM16E-mediated macropinocytosis promotes cell survival under acidic stress.

Cellular and molecular life sciences : CMLS·2026
Same author

Heat- and PIP2-dependent TRPM4 activity underlies mutually exclusive human diseases.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Kv7 Channels as an Important Contributor to Alcohol-Induced Modulation of Neuronal Excitability in Neonatal Rat Superior Cervical Ganglion.

Cells·2025
Same author

Palmitoylation Code and Endosomal Sorting Regulate ABHD17A Plasma Membrane Targeting and Activity.

International journal of molecular sciences·2025
Same author

A brief history of nerve action potentials after 1600.

Molecular pharmacology·2025

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • KCNQ (Kv7) channels are crucial for neuronal excitability and are regulated by phosphatidylinositol 4,5-bisphosphate (PIP(2)).
  • Muscarinic receptors can modulate KCNQ channel activity through phospholipase C (PLC) activation, which cleaves PIP(2).

Purpose of the Study:

  • To investigate the role of diacylglycerols (DAGs) in the muscarinic regulation of KCNQ2/KCNQ3 channels.
  • To determine if DAGs or their downstream products mediate the suppression of KCNQ currents.

Main Methods:

  • Electrophysiology was used to measure KCNQ currents in tsA cells.
  • Fluorescent translocation probes monitored PIP(2) and DAG levels.
  • Cells were transfected with M(1) muscarinic receptors, KCNQ2/KCNQ3 subunits, and probes.

Related Experiment Videos

  • Pharmacological agents inhibited DAG metabolism (DAG kinase, DAG lipase) or mimicked DAG effects.

    • Main Results:

    • Exogenous DAGs and phorbol esters did not affect KCNQ current suppression by muscarinic agonists.
    • Inhibiting DAG metabolism (DAG kinase or lipase) did not alter muscarinic regulation or current recovery.
    • DAGs and their metabolites are not essential for acute muscarinic modulation of KCNQ channels.

    Conclusions:

    • Diacylglycerols generated by PLC activation are not critical for the acute muscarinic modulation of KCNQ channels.
    • Protein kinase C activation downstream of DAG is also not essential for this regulatory pathway.
    • The study clarifies the signaling mechanisms underlying KCNQ channel regulation by muscarinic receptors.