Estrogen transiently increases delayed rectifier, voltage-dependent potassium currents in ovine gonadotropes

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Treatment of gonadotropes with estrogen (E) changes the electrophysiological response to gonadotropin-releasing hormone (GnRH) such that the cells are hyperpolarised immediately after stimulation with GnRH and then generate action potentials more frequently than non-E-treated cells. We investigated the role of K+ current in this altered response to GnRH using cultures of ewe pituitary cells enriched for gonadotropes. K+ current density was measured using nystatin-perforated whole-cell recordings in the voltage clamp mode. Treatment of cells with E for 16-20 h significantly (p < 0.01) increased the unit K+ current to 180% of that in vehicle-treated cells. Outward current in these cells flows predominantly through voltage-dependent, delayed rectifier K+ channels (I(K)), and E alters the magnitude of this current. The effect of E to increase the K+ current was dose- and time-dependent and was maximal after 16-20 h. The unit K+ current values returned to pre-treatment levels after 36 h of E treatment. Several cells were studied both before and after E treatment and the average effect of E on these cells was to increase the unit K+ current by 90%. The time-course of the effect of E on K+ current density is the same as the effect of E to increase LH release in vitro and in vivo. We conclude that the increase in K+ current may be an important part of the mechanism whereby E acts on gonadotropes to facilitate the LH surge which triggers ovulation.

Original languageEnglish
Pages (from-to)254-260
Number of pages7
Issue number4
Publication statusPublished - 1 Jan 1999


  • Electrophysiology
  • Gonadal steroids
  • Gonadotrope
  • Gonadotropin-releasing hormone
  • Gonadotropins
  • Ovine
  • Potassium channels

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