Effects of Ovariectomy and Sex Steroids on Prolactin Synthesis

Prolactin (PRL) plays a variety of roles to maintain female reproductive functions. In female rats, <i>Prl</i> mRNA expression in the anterior pituitary was significantly suppressed by OVX. The OVX-induced inhibition of PRL expression was recovered by estradiol (E2) supplementation after OVX. Supplementation of progesterone (P4) and the androgen dihydrotestosterone (DHT) did not prevent the OVX-induced decrease of PRL expression. When E2 was administered to ovary-intact rats, <i>Prl</i> expression was significantly increased, but neither P4 nor DHT modulated its expression. In experiments using the PRL-producing GH3 cell line, a higher concentration of E2 significantly increased <i>Prl</i> expression; however, neither P4 nor DHT modulated its expression in these cells. Gene expression of thyrotropin-releasing hormone (TRH), a PRL-releasing factor within the hypothalamus, was unchanged by OVX. Similarly, OVX had no effect on the hypothalamic expression of the gene encoding tyrosine hydroxylase, a marker of dopamine that inhibits PRL. In addition, mRNA expression of TRH receptor and dopamine D2 receptor did not change by OVX within the pituitary. Moreover, the expression of follistatin (<i>Fst</i>) mRNA was increased following OVX and decreased with E2 supplementation in the anterior pituitary. However, FST had no effect on TRH-induced PRL synthesis. Our current observations suggest that the OVX-induced reduction of PRL principally depends on the depletion of E2. E2 has a direct effect on PRL-producing lactotrophs and increases PRL levels without affecting hypothalamic PRL-releasing/inhibiting factors.