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Dexamethasone-mediated inhibition of calcium transients and ACTH release in a pituitary cell line (AtT-20)

K J Loechner1, R J Knox, J T McLaughlin

  • 1Department of Physiology, Tufts University School of Medicine, Boston, MA 02111, USA. Loechnek@musc.edu

Steroids
|August 5, 1999
PubMed

Insights

Dexamethasone reduces calcium levels in pituitary cells, but this effect does not explain its inhibition of adrenocorticotropic hormone release. Further research is needed to understand dexamethasone

Area of Science:

  • Endocrinology
  • Cell Biology
  • Neuroscience

Background:

  • Adrenocorticotropic hormone (ACTH) release from pituitary corticotrophs is stimulated by corticotropin-releasing hormone (CRH) and inhibited by dexamethasone.
  • The exact mechanisms underlying dexamethasone's inhibitory effect on ACTH secretion remain unclear.
  • Calcium homeostasis is a critical regulator of hormone release in pituitary cells.

Purpose of the Study:

  • To investigate whether dexamethasone modulates ACTH release by regulating calcium homeostasis in AtT-20 cells.
  • To evaluate the specific effects of dexamethasone on calcium currents, intracellular calcium concentrations, and ACTH release.
  • To determine the relationship between dexamethasone's impact on calcium influx and its inhibition of ACTH secretion.

Main Methods:

  • Utilized perforated patch-clamp electrophysiology to measure calcium currents in AtT-20 cells.
  • Employed calcium imaging with fura PE3/AM to assess intracellular calcium levels.
  • Administered dexamethasone and calcium channel antagonists (nifedipine, omega-agatoxin IVA) to evaluate their effects on calcium dynamics and ACTH release.

Main Results:

  • Dexamethasone significantly decreased both calcium currents and intracellular calcium levels in AtT-20 cells.
  • The inhibitory effect of dexamethasone on calcium currents was independent of L-type and P/Q-type calcium channel blockade.
  • While prolonged dexamethasone treatment (2 h) inhibited CRH-induced ACTH release by approximately 40%, a rapid 10-minute incubation did not affect release, despite inhibiting calcium transients.

Conclusions:

  • Dexamethasone does modulate calcium homeostasis in AtT-20 pituitary cells by reducing calcium influx.
  • The observed modulation of calcium homeostasis by dexamethasone is not the primary mechanism responsible for its inhibition of ACTH secretion.
  • Further investigation is required to elucidate the precise molecular pathways through which dexamethasone exerts its inhibitory control over ACTH release.

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