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Abstract
Thyrotropin-releasing hormone (TRH) stimulates biphasic prolactin (PRL) secretion from rat pituitary GH 3 cells. The pretreatment of cells with EGTA (100 μM) plus arachidonic acid (15 μM), a condition which decreased TRH-responsive intracellular Ca 2+ pools, eliminated the activity of TRH on burst PRL secretion (2 min) but did not alter that on sustained PRL secretion (30 min). However, the treatment of cells with EGTA, arachidonic acid and H-7 (300 μM), a potent inhibitor of protein kinase C (PKC), almost completely suppressed the activity of TRH for sustained PRL secretion. In cells down-modulated for PKC, TRH abolished this Ca 2+-independent sustained PRL secretion. These results suggest that TRH acts through a separate, Ca 2+-independent secretory mechanism, besides by modulating the Ca 2+-dependent mechanism and that PKC is involved in this Ca 2+-independent secretory pathway.
Published Version
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