Stimulation of Prolactin Secretion by Estrogens and Androgens in PMS-HCG Treated Immature Rats

Abstract

Beginning at 26 days of age, immature female rats were given the PMS-HCG treatment recommended by Parlow (1958) for preparing rats for the OAAD test for LH. The time course of changes in ovarian and uterine weight and in serum and pituitary levels of prolactin was followed from Day 30 to Day 37. Both ovarian and uterine weights declined rapidly beginning on Day 32, whereas a decline in pituitary and serum levels of prolactin began on Days 30 and 31, respectively. It was concluded that the drop in serum prolactin was probably the major cause of the regression in ovarian weight. Several groups of PMS-HCG treated animals were treated daily from Days 30–36 with 17β estradiol (E2), 17β estradiol benzoate (EB), dehydroepiandrosterone (DHA), testosterone propionate (TP), or 5α-dihydrotestosterone and sacrificed on Day 37. Analysis of ovarian weights showed that both estrogens and those androgens which can undergo conversion to estrogens (i.e., DHA and TP) maintained ovarian weight at the level seen in the PMS-HCG-treated controls on Day 32. Likewise, these same steroids all produced a highly significant elevation in both the serum and pituitary concentrations of prolactin. In contrast, 5α-dihydrotestosterone, an androgen which does not undergo aromatization to estrogens was without effect on ovarian weight or in altering either serum or pituitary levels of prolactin. Thus, it was concluded that either estrogens or androgens which can undergo conversion to estrogens are capable of stimulating prolactin secretion in immature, PMS-HCG treated female rats.