To determine the capacity of the rat ovary to produce 5α-androstane-3α, 17β-diol (α-diol) in response to gonadotropins during the time of puberty, the ovaries of animals at different phases of puberty were incubated in vitro in the presence of hCG, and the 3α-diol released into the medium was measured by RIA. Basal 3α-diol release, i.e. in the absence of hCG, did not change appreciably throughout puberty. In contrast, the 3α-diol release in response to hCG was elevated in late juvenile rats (32 days of age, anestrous phase of puberty) and during early puberty (early proestrous phase), but declined markedly on the morning of the first proestrous day (late proestrous phase). The response reached minimal values on the day of first estrus and remained low on the first diestrus. Since the 3α-diol release in response to hCG declined before the first preovulatory surge of gonadotropins, at a time in which serum gonadotropin levels are low but the serum levels of PRL are increasing, the effect of hyper- and hypoprolactinemia on the response of the steroid to hCG was evaluated in 31–32-day-old rats. Serum PRL levels were elevated by treating the animals with sulphide, a dopaminergic receptor blocker, and hypoprolactinemia was induced by treatment with bromoergocriptine (CB-154), a dopaminergic receptor agonist. The ovarian release of 3αdiol in response to hCG in vitro was significantly reduced in hyperprolactinemic animals and markedly elevated in PRL-deficientrats.The results indicate that the production of 3α-diol by the prepubertal ovary in response to hCG in vitro decreases during the hours preceding the first preovulatory surge of gonadotropins. Since serum PRL levels increase unambiguously during the days antedating the first proestrus, and because the release of 3α-diol from the ovary in! response to hCG, i in vitro was found to be influenced by experimentally-induced changes in serum PRL titers, it is suggested that the prepubertal decline in ovarian 3αdiol response to hCG is, at least in part, a PRL-dependent phenomenon. 223, 1981) response to hCG is, at least in part, a PRL-dependent phenomenon.
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