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J Biol Chem, Vol. 274, Issue 11, 7508-7515, March 12, 1999

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. CharlesDagger , Elemer T. Piros, Chris J. Evansparallel , and Tim G. Hales**

From the Dagger  Department of Neurology, UCLA School of Medicine, Los Angeles, California 90095,  Department of Physiology, Cornell University, New York, New York 10021, parallel  Department of Psychiatry, Neuropsychiatric Institute, UCLA School of Medicine, Los Angeles, California 90095, and ** Department of Pharmacology, The George Washington University, Washington, D. C. 20037

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-trisphosphate-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 (KIR) 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, KCa,V) and increased the amplitude of Ca2+ oscillations. Ba2+ inhibited both KIR and KCa,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 KIR channels modulate the frequency of Ca2+ oscillations and prolactin release, whereas TEA-sensitive KCa,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.

Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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