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Ionic mechanisms underlying TRH-induced prolactin secretion in rat lactotrophs

J R Schwarz1, C K Bauer

  • 1Abteilung für angewandte Physiologie, Universität Hamburg, Germany.

Rossiiskii Fiziologicheskii Zhurnal Imeni I.M. Sechenova
|July 2, 1999
PubMed

Insights

Thyrotropin-releasing hormone (TRH) increases prolactin secretion by modulating an inward-rectifying K current (IK, IR) in pituitary cells. This ERG-like current maintains resting potential and influences TRH effects.

Area of Science:

  • Neuroendocrinology
  • Molecular Physiology
  • Ion Channel Physiology

Background:

  • Thyrotropin-releasing hormone (TRH) stimulates prolactin secretion from pituitary cells.
  • An inward-rectifying potassium current (IK, IR) is implicated in TRH-induced prolactin release.
  • The specific molecular identity and function of this IK, IR remain to be fully elucidated.

Purpose of the Study:

  • To characterize the inward-rectifying K current (IK, IR) in GH3/B6 pituitary cells.
  • To determine the molecular basis of IK, IR using heterologous expression.
  • To investigate the role of IK, IR in TRH-mediated prolactin secretion.

Main Methods:

  • Whole-cell patch-clamp electrophysiology in GH3/B6 cells and CHO cells.
  • Pharmacological isolation of IK, IR using the ERG channel blocker E-4031.
  • Heterologous expression of the rat ERG channel homolog (RERG) in CHO cells.

Main Results:

  • The IK, IR in GH3/B6 cells exhibited properties identical to channels encoded by RERG.
  • TRH significantly reduced the outward component of the ERG-like current (IK, IR) at physiological potentials.
  • Blocking IK, IR mimicked the TRH-induced depolarization and increased Ca action potential frequency.

Conclusions:

  • The ERG-like current (IK, IR) in GH3/B6 cells contributes to maintaining resting membrane potential.
  • This current plays a crucial role in the mechanism by which TRH enhances prolactin secretion.
  • RERG channels are likely responsible for the observed IK, IR in these pituitary cells.

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