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GABA-activated Single-channel and Tonic Currents in Rat Brain Slices
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Published on: July 17, 2011

Tubocurarine blocks a calcium-dependent potassium current in rat tumoral pituitary cells

P Vacher1, A M Vacher, P Mollard

  • 1Laboratory of Neurophysiology, CNRS UMR 5543 University V. Segalen, Bordeaux, France.

Molecular and Cellular Endocrinology
|August 15, 1998
PubMed

Insights

Potassium channel inhibitors like d-tubocurarine and TEA reveal distinct calcium-dependent potassium currents in pituitary cells. These currents influence electrical activity and hormone release, with d-tubocurarine specifically targeting the slow current.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Pituitary GH3/B6 cells exhibit complex electrical activity involving ion channels.
  • Understanding potassium currents is crucial for deciphering cellular signaling and hormone secretion.

Purpose of the Study:

  • To investigate the effects of potassium channel inhibitors on electrical activity, ionic currents, intracellular calcium, and hormone release in GH3/B6 cells.
  • To characterize the distinct roles of different calcium-activated potassium currents (I AHPs and I AHPf) in these cells.

Main Methods:

  • Patch-clamp electrophysiology (current clamp and voltage-clamp) was used to record electrical activity and ionic currents.
  • Intracellular calcium concentration ([Ca2+]i) was monitored.
  • The effects of potassium channel inhibitors, including d-tubocurarine (dTc) and tetraethylammonium ions (TEA+), were assessed.

Main Results:

  • GH3/B6 cells display two distinct calcium-dependent potassium currents (I AHPs and I AHPf) with different kinetics and pharmacological profiles.
  • D-tubocurarine selectively suppressed the slow current (I AHPs), while TEA+ blocked the fast current (I AHPf).
  • Both dTc and TEA+ increased calcium influx and stimulated prolactin and growth hormone release.

Conclusions:

  • GH3/B6 cells possess at least two distinct calcium-dependent potassium currents that differentially shape action potentials.
  • The slow current (I AHPs) is sensitive to subplasmalemmal calcium changes and can be pharmacologically targeted by d-tubocurarine.
  • Inhibition of these potassium currents stimulates pituitary hormone release, highlighting their role in regulating secretion.

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