RAT PLACENTAL LACTOGEN-I ABOLISHES NOCTURNAL PROLACTIN SURGES IN THE PREGNANT RAT

The twice-daily surges of prolactin (PRL) present during the first hal f of pregnancy abruptly terminate at midpregnancy concurrent with the appearance of high levels of placental lactogen-I (PL-I) in the blood. This study addressed the role PL-I and other pituitary or placental h ormones have in terminating PRL surges in pregnant rats. Implantation of rat PL-I (rPL-I) or ovine PRL into the arcuate-median eminence area of the hypothalamus of day 7 pregnant rats totally eliminated nocturn al PRL surges on days 8 and 9. To assess the specificity of the inhibi tory effects of hormones from the PRL-growth hormone (CH) family, rat growth hormone (rGH), human growth hormone (hGH), and rat prolactin-li ke protein-A (PLP-A) were tested. Only the lactogenic hormone, hGH, ha d any effect. Since lactogenic hormones may inhibit PRL by stimulation of dopamine synthesis and release into the hypophysial portal blood v essels leading to the anterior pituitary, the effect of these hormones on tyrosine hydroxylase (TH), the rate-limiting enzyme for the synthe sis of dopamine activity, was determined. In pregnant rats, both ovine prolactin (oPRL) and hGH significantly increased (64%) TH activity, w hereas rPL-I was less effective. In ovariectomized, bromocriptine-trea ted rats, both rPL-I and oPRL increased TH activity 207 and 151%, resp ectively, This supports the concept that termination of PRL surges at midpregnancy are owing to secretion of placental lactogens (PLs) from the placenta, However, the mechanism for the inhibition cannot be enti rely attributed to an increase in tuberoinfundibular dopaminergic neur onal activity.