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J Biol Chem, Vol. 274, Issue 11, 7508-7515, March 12, 1999
From the 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.
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
,
, and
Department of Neurology, UCLA School of
Medicine, Los Angeles, California 90095, ¶ Department of
Physiology, Cornell University, New York, New York 10021,
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
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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