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

Receptor-mediated modulation of recombinant neuronal class E calcium channels

G Mehrke1, A Pereverzev, H Grabsch

  • 1Institute of Neurophysiology, University of Köln, Germany.

FEBS Letters
|May 26, 1997
PubMed
Summary

Somatostatin inhibits neuronal calcium channel currents via pertussis toxin-sensitive G-proteins. This modulation occurs independently of a specific C-terminal fragment in the alpha1Ed calcium channel subunit.

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

Cav2.3 R-type calcium channels: from its discovery to pathogenic de novo CACNA1E variants: a historical perspective.

Pflugers Archiv : European journal of physiology·2020
Same author

In vitro and in vivo phosphorylation of the Ca<sub>v</sub>2.3 voltage-gated R-type calcium channel.

Channels (Austin, Tex.)·2018
Same author

A practical guide to the preparation and use of metal ion-buffered systems for physiological research.

Acta physiologica (Oxford, England)·2017
Same author

Medium-chain fatty acids modulate myocardial function via a cardiac odorant receptor.

Basic research in cardiology·2017
Same author

Differences in the Early Development of Human and Mouse Embryonic Stem Cells.

PloS one·2015
Same author

R-Type Voltage-Gated Ca²⁺ Channels in Cardiac and Neuronal Rhythmogenesis.

Current molecular pharmacology·2015

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Neuronal calcium channels are crucial for nerve function.
  • Understanding their modulation is key to developing new therapeutics.
  • The alpha1E calcium channel subtype plays a significant role in neuronal excitability.

Purpose of the Study:

  • To investigate the signaling pathways involved in the modulation of the human alpha1Ed calcium channel.
  • To determine the role of G-proteins in somatostatin's inhibitory effect on neuronal calcium currents.
  • To examine whether the C-terminal splice variant influences somatostatin's action.

Main Methods:

  • Stable transfection of human embryonic kidney (HEK293) cells with alpha1Ed cDNA.
  • Electrophysiological recordings (inward currents) of calcium and barium ions.

Related Experiment Videos

  • Application of somatostatin, carbachol, ATP, adenosine, pertussis toxin, GDP-beta-S, and GTP-gamma-S.

    • Main Results:

    • Somatostatin, carbachol, ATP, and adenosine inhibited alpha1Ed-mediated currents and slowed inactivation.
    • The inhibitory effect of somatostatin was significantly reduced by pertussis toxin pre-incubation.
    • G-protein modulators (GDP-beta-S, GTP-gamma-S) attenuated the somatostatin effect.
    • Somatostatin inhibited currents in cells expressing both full-length and truncated alpha1Ed subunits.

    Conclusions:

    • Modulation of the alpha1Ed calcium channel by somatostatin involves pertussis toxin-sensitive G-proteins.
    • The C-terminal 129-bp fragment does not influence the inhibitory action of somatostatin.
    • These findings elucidate the signaling mechanism of somatostatin on a specific neuronal calcium channel subtype.