Blocking K+ channels with TEA induces plasmalemma depolarization, increased [Ca2+]i, and ACTH secretion in AtT-20

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X Wang1, M A Greer

  • 1Department of Physiology, Oregon Health Sciences University, Portland 97201, USA.

Molecular and Cellular Endocrinology
|March 1, 1995
PubMed

Insights

Blocking potassium (K+) channels with tetraethylammonium (TEA) triggers ACTH secretion in pituitary cells. This occurs via membrane depolarization, calcium influx, and subsequent hormone release, revealing a key regulatory mechanism.

Area of Science:

  • Endocrinology
  • Neuroscience
  • Cell Biology

Background:

  • Potassium (K+) channel blockade is known to induce hormone secretion in pituitary cells.
  • The precise mechanism underlying this phenomenon remains incompletely understood.

Purpose of the Study:

  • To investigate the mechanism by which K+ channel blockade by tetraethylammonium (TEA) induces ACTH secretion in AtT-20 mouse pituitary cells.
  • To correlate the effects of TEA on K+ currents, membrane potential, intracellular calcium ([Ca2+]i), and ACTH release.

Main Methods:

  • Whole-cell patch-clamp recording to measure K+ currents and membrane potential.
  • Fura-2 fluorescence to quantify cytosolic Ca2+ ([Ca2+]i) concentration.
  • Perifusion system to measure ACTH secretion.

Main Results:

  • TEA inhibited voltage-dependent K+ currents and caused dose-dependent membrane depolarization.
  • TEA induced a concentration-dependent increase in [Ca2+]i and ACTH secretion.
  • Both TEA-induced [Ca2+]i rise and ACTH secretion were dependent on extracellular calcium.

Conclusions:

  • TEA-induced pituitary hormone secretion is mediated by K+ channel blockade, membrane depolarization, and subsequent calcium influx.
  • These findings highlight the critical role of K+ channel regulation in controlling pituitary hormone release.

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