The number of plasma membrane receptors for TRH on tumor-derived mammotropic cells in culture, GH3 and GC cells, but not their affinity for TRH, was increased by estrogens. For GH3 cells, exposure to 10 nM 17 beta-estradiol for 48 h increased the receptor level from 54,000 to 90,000 sites/cell, while for GC cells, the number of receptors increased from 29,000 to 46,000 after 28 h. PRL accumulation in the medium was also increased by 17 beta-estradiol. 17 beta-Estradiol and diethylstilbestrol were equally potent in increasing the TRH receptor level, while estrone was only 1/10th as potent. Diethylstilbestrol bound to the cytoplasmic estrogen receptor with an apparent affinity approximately 2.5 times higher than 17 beta-estradiol in GH3 and GC cells, while the affinity for estrone was only 1/12th to 1/20th that of 17 beta-estradiol. Tamoxifen, an antiestrogenic compound, inhibited the increase in TRH receptor number induced by 0.3 nM 17 beta-estradiol and was capable of binding to the estrogen receptor. Modulation of the TRH receptor level on mammotropic cells by estrogens, which is likely mediated through cytoplasmic estrogen receptors, may be an important mechanism for regulation of TRH action.
A B S T R A C T 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 Ca21 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
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