Abstract
Prolactin (PRL) plays a variety of roles to maintain female reproductive functions. In female rats, Prl 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, Prl 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 Prl 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 (Fst) 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.