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Free access | 10.1172/JCI110216

Thyrotropin-releasing Hormone Stimulation of Prolactin Release from Clonal Rat Pituitary Cells: EVIDENCE FOR ACTION INDEPENDENT OF EXTRACELLULAR CALCIUM

Marvin C. Gershengorn, Sylvia T. Hoffstein, Mario J. Rebecchi, Elizabeth Geras, and Brian G. Rubin

Department of Medicine, New York University Medical Center, New York, New York 10016

Find articles by Gershengorn, M. in: PubMed | Google Scholar

Department of Medicine, New York University Medical Center, New York, New York 10016

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Department of Medicine, New York University Medical Center, New York, New York 10016

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Department of Medicine, New York University Medical Center, New York, New York 10016

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Department of Medicine, New York University Medical Center, New York, New York 10016

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Published June 1, 1981 - More info

Published in Volume 67, Issue 6 on June 1, 1981
J Clin Invest. 1981;67(6):1769–1776. https://doi.org/10.1172/JCI110216.
© 1981 The American Society for Clinical Investigation
Published June 1, 1981 - Version history
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Abstract

Thyrotropin-releasing hormone (TRH) stimulates prolactin release and 45Ca2+ efflux from GH3 cells, a clonal strain of rat pituitary cells. Elevation of extracellular K+ also induces prolactin release and increases 45Ca2+ efflux from these cells. In this report, we distinguish between TRH and high K+ as secretagogues and show that TRH-induced release of prolactin and 45Ca2+ is independent of the extracellular Ca2+ concentration, but the effect of high K+ on prolactin release and 45Ca2+ efflux is dependent on the concentration of Ca2+ in the medium. The increment in 45Ca2+ efflux induced by 50 mM K+ during perifusion was reduced in a concentration-dependent manner by lowering extracellular Ca2+ from 1,500 to 0.02 μM (by adding EGTA), whereas 1 μM TRH enhanced 45Ca2+ efflux similarly over the entire range of extracellular Ca2+ concentrations. Although 50 mM K+ caused release of 150 ng prolactin from 40 × 106 GH3 cells exposed to 1,500 μM Ca2+ (control), reduction of extracellular Ca2+ to 2.8 μM decreased prolactin release caused by high K+ to <3% of controls and no prolactin release was detected after exposure to 50 mM K+ in medium with 0.02 μM free Ca2+. In contrast, TRH caused release of 64 ng of prolactin from 40 × 106 GH3 cells exposed to medium with 1,500 μM Ca2+, and release caused by TRH was still 50 and 35% of control in medium with 2.8 and 0.02 μM Ca2+, respectively. Furthermore, TRH transiently increased by 10-fold the fractional efflux of 45Ca2+ from GH3 cells in static incubations with 1,500 or 3.5 μM Ca2+, hereby confirming that the enhanced 45Ca2+ efflux caused by TRH in both low and high Ca2+ medium was not an artifact of the perifusion system.

Data obtained with chlortetracycline (CTC), a probe of membrane-bound Ca2+, were concordant with those obtained by measuring 45Ca2+ efflux. Cellular fluorescence of CTC varied with the extracellular Ca2+ concentration and the duration of incubation. TRH decreased the fluorescence of cell-associated CTC in a manner strongly suggesting stimulus-induced mobilization of Ca2+, and this effect was still demonstrable in GH3 cells incubated in 50 mM K+.

These data suggest that TRH acts to mobilize sequestered cell-associated Ca2+ reflected as a 45Ca2+ efflux which is independent of the extracellular Ca2+ concentration. Mobilization of sequestered Ca2+ into the cytoplasm may elevate free intracellular Ca2+ and serve to couple stimulation by TRH to secretion of prolactin.

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