The purpose of this study was to determine the effects of the light-dark cycle, adrenal glands and steroid treatment schedule on LH and prolactin release in rats. Rats maintained in either a 14 h light: 10 h dark schedule (LD) or constant illumination (LL) were ovariectomized (Ovx) or ovariectomized and adrenalectomized (Ovx-Adx). Three weeks later at 1000 h, animals received a SC injection of estradiol benzoate (EB 10 mug/100 g BW) or oil. Three days after EB administration, rats were given a 2 mg injection of progesterone (P) or oil at either 0200, 0500, or 0900 h, and were sequentially bled at four-hour intervals until 1700 h. P administered at all three times increased the amplitude of the plasma LH surge and advanced it, though by no more than 4 hours, in LD. In LL, P was more effective in advancing the time of LH release, although peak plasma LH levels were considerably less than those observed in LD. Adrenalectomy increased the sensitivity of Ovx rats to the effects of EB and P on LH release. P administration at either 0200, 0500 or 0900 h advanced prolactin release in EB-primed Ovx and Ovx-Adx in LL and LD, but only in LL did P increase the amplitude of the plasma prolactin surge. The lighting conditions did not alter the effectiveness of P in advancing prolactin release. Our study demonstrates that the light-dark cycle and adrenal steroids interact to synchronize the timing of LH release in rats, but the regulatory mechanism controlling prolactin release is less strictly cued to these environmental factors.

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The effects of neonatal cortisol acetate administration on diurnal changes in serum corticosterone, progesterone and LH and on the response to pregnant mare serum gonadotrophin (PMSG) were examined in immature female rats. Neonatal cortisol treatment (250 micrograms/rat) abolished the diurnal rhythm of serum progesterone in rats at 27-29 days of age, and lowered overall the serum progesterone response to PMSG. Neonatal cortisol also reduced the number of animals ovulating on day 28 after PMSG injection 48 h earlier. This dosage of cortisol did not alter the diurnal rhythm of serum corticosterone in these animals. Serum LH concentrations in control rats at 27-29 days of age did not differ between 09.00 and 18.00 h, and prior treatment with cortisol acetate did not significantly influence serum concentrations of this hormone. Our data suggest that ovarian production of progesterone contributes significantly to diurnal fluctuations of this steroid in the circulation of immature rats. Perinatal exposure to cortisol acetate abolishes the diurnal rhythm of serum progesterone and impairs the ovarian response of the immature female rat to PMSG. The mechanism(s) by which cortisol acetate alters these processes remains to be determined.