Apamin-sensitive potassium channels mediate agonist-induced oscillations of membrane potential in pituitary gonadotrophs

FEBS Lett. 1992 Apr 13;301(1):19-22. doi: 10.1016/0014-5793(92)80201-q.

Abstract

In cultured rat pituitary gonadotrophs, gonadotropin-releasing hormone (GnRH) induces rapid hyperpolarization of the cell membrane and causes cessation of the spontaneous electrical activity present in non-stimulated cells. This initial response to GnRH is followed by slow oscillations of membrane potential (Vm) which often exhibit brief bursts of action potentials (AP) fired from the peak of the oscillations. The hyperpolarization waves are synchronous with GnRH-induced elevations of cytoplasmic Ca2+ concentration ([Ca2+]i), such that Vm maxima alternate with the peak values of [Ca2+]i. The Vm oscillations result from repetitive activation of apamin-sensitive K+ channels by cytoplasmic Ca2+. Thus, GnRH activation of Ca2+ mobilization can generate a bursting pattern of membrane potential through the activation of K+ channels against a background of spontaneous electrical activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apamin / pharmacology*
  • Calcium / metabolism
  • Calcium Channels / metabolism
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Female
  • Gonadotropin-Releasing Hormone / pharmacology*
  • Membrane Potentials / physiology*
  • Microelectrodes
  • Pituitary Gland / drug effects
  • Pituitary Gland / metabolism*
  • Potassium / metabolism
  • Potassium Channels / drug effects
  • Potassium Channels / metabolism*
  • Rats

Substances

  • Calcium Channels
  • Potassium Channels
  • Apamin
  • Gonadotropin-Releasing Hormone
  • Potassium
  • Calcium