L-type Ca2+ channels and K+ channels specifically modulate the frequency and amplitude of spontaneous Ca2+ oscillations and have distinct roles in prolactin release in GH3 cells

Andrew C. Charles, Elemer T. Piros, Chris J. Evans, Tim G. Hales

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

GH3 cells showed spontaneous rhythmic oscillations in intracellular calcium concentration ([Ca2+](i)) and spontaneous prolactin release. The L- type Ca2+ channel inhibitor nimodipine reduced the frequency of Ca2+ oscillations at lower concentrations (100nM-1 μM), whereas at higher concentrations (10 μM), it completely abolished them. Ca2+ oscillations persisted following exposure to thapsigargin, indicating that inositol 1,4,5- triphosphate-sensitive intracellular Ca2+ stores were not required for spontaneous activity. The K+ channel inhibitors Ba2+, Cs+, and tetraethylammonium (TEA) had distinct effects on different K+ currents, as well as on Ca2+ oscillations and prolactin release. Cs+ inhibited the inward rectifier K+ current (K(1R)) and increased the frequency of Ca2+ oscillations. TEA inhibited outward K+ currents activated at voltages above -40 mV (grouped within the category of Ca2+ and voltage-activated currents, K(Ca,V)) and increased the amplitude of Ca2+ oscillations. Ba2+ inhibited both K(1R) and K(Ca,V) and increased both the amplitude and the frequency of Ca2+ oscillations. Prolactin release was increased by Ba2+ and Cs+ but not by TEA. These results indicate that L-type Ca2+ channels and K(1R) channels modulate the frequency of Ca2+ oscillations and prolactin release, whereas TEA-sensitive K(Ca,V) channels modulate the amplitude of Ca2+ oscillations without altering prolactin release. Differential regulation of these channels can produce frequency or amplitude modulation of calcium signaling that stimulates specific pituitary cell functions.

Original languageEnglish
Pages (from-to)7508-7515
Number of pages8
JournalJournal of Biological Chemistry
Volume274
Issue number11
DOIs
Publication statusPublished - 12 Mar 1999

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