Maturation of the control of gonadotropin and prolactin release in the rat

Several aspects of the maturation of the control of pituitary gonadotropin and prolactin secretion in the rat have been studied. Circulating estrogen (E₂) titers were found to be elevated in the infantile female, declining as the animal approached maturity. These high E₂ levels appear to be due to an enhanced E₂ production by the ovaries and adrenals and to a reduced metabolic degradation of the steroid. High plasma FSH titers in the presence of elevated E₂ levels in infantile rats were found to be caused at least in part by a decreased effectiveness of the estrogen negative feedback and by an increased pituitary responsiveness to LH RH induced by a direct action of progesterone and 5α dihydrotestosterone on the gland. Negative estrogen feedback controlling LH secretion was also decreased in infantile rats and pituitary responsiveness to LH RH enhanced. This latter phenomenon, however, was not altered by ovariectomy adrenalectomy or by steroid(s) replacement therapy. The decline in plasma gonadotropins observed after day 15 was found to be caused at least in part by a decrease in pituitary responsiveness to LH RH and by an increased effectiveness of estrogen negative feedback. This feedback becomes fully competent during the days preceding the onset of puberty. At puberty estrogen secretion gradually increases to reach levels that, by exerting a positive feedback action, trigger a preovulatory peak of gonadotropins and prolactin. Pituitary responsiveness to LH RH increased the day before the first ovulation, presumably due to the elevated E₂ levels present and to a direct effect of LH RH that, by acting on the gland, sensitized it to its own action. Lastly, the inhibitory dopaminergic (DA) control of prolactin secretion was found to be more pronounced in female than in male rats. This difference appeared to be due to a modulatory action of estogen initiated at a pre pubertal age rather than to a process of neonatal hypothalamic sexual differentiation. In the female the inhibitory DA control of prolactin is initiated shortly after birth, whereas the stimulatory effect of estrogen on prolactin release develops after the third week of post natal life, reaching a maximum around the time of puberty. It seems that in both male and female, tonic prolactin release depends on the balance between the inhibitory DA tone and the influence of stimulatory signals. Increased stimulation of prolactin release would be followed by a compensatory increase in the inhibitory DA tone to attenuate the prolactin response.