Estrogen control of prolactin synthesis in vitro.
Primary cultures of rat pituitary cells respond to estradiol-17beta by increased incorporation of radiolabeled precursors into prolactin but not into the bulk of other cellular proteins. The rate of increase in prolactin synthesis is dose dependent, reaching maximal levels in the physiological range of estradiol. At a concentration of 1 nM, estradiol, diethylstilbestrol, and estriol are stimulatory whereas androgens, progesterone, and corticosterone are without significant effect. Exposure of pituitary cells to 10 nM estradiol resulted in a 500% increase in prolactin synthesis after 7 days of culture. The results indicate that estradiol can stimulate prolactin synthesis through direct action on the pituitary.
D000728:Androgens / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D003345:Corticosterone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D007700:Kinetics; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology; D011388:Prolactin / Q000096:biosynthesis*; D051381:Rats; D013329:Structure-Activity Relationship
D000728:Androgens; D004967:Estrogens; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin; D003345:Corticosterone