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Calcium currents in a pituitary cell line (AtT-20): differential roles in stimulus-secretion coupling

K J Loechner1, R M Kream, K Dunlap

  • 1Department of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.

Endocrinology
|April 1, 1996
PubMed

Insights

Dihydropyridine-sensitive calcium channels control ACTH release in mouse pituitary cells. Other calcium channel subtypes and toxin-resistant currents do not significantly impact adrenocorticotropic hormone (ACTH) release.

Area of Science:

  • Neuroendocrinology
  • Cellular Physiology

Background:

  • Adrenocorticotropic hormone (ACTH) release is crucial for stress response.
  • Voltage-dependent calcium channels (VDCCs) play a role in hormone secretion from pituitary cells.

Purpose of the Study:

  • To identify specific VDCC subtypes regulating ACTH release from AtT-20 cells.
  • To determine the contribution of different calcium channel populations to stimulated ACTH secretion.

Main Methods:

  • Perforated patch-clamp electrophysiology to identify calcium currents.
  • Radioimmunoassay (RIA) to quantify ACTH release.
  • Pharmacological characterization using channel blockers like nimodipine, omega-Agatoxin IVA, omega-Conotoxin MVIIC, omega-Conotoxin GVIA, and cadmium.

Main Results:

  • AtT-20 cells exhibit nimodipine-, omega-Agatoxin IVA-, and omega-Conotoxin MVIIC-sensitive calcium currents, but not omega-Conotoxin GVIA-sensitive currents.
  • A cadmium-sensitive, toxin-resistant current was also observed.
  • Nimodipine significantly inhibited ACTH release stimulated by corticotropin-releasing hormone (CRH) or potassium chloride (KCl).
  • Other calcium channel blockers and the toxin-resistant current did not significantly affect ACTH release.

Conclusions:

  • Dihydropyridine-sensitive calcium channels are the primary mediators of CRH- or KCl-stimulated ACTH release in AtT-20 cells.
  • Other identified calcium channel subtypes and the toxin-resistant current are not significantly coupled to ACTH secretion in this model.

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