Stimulatory versus Inhibitory Effects of Progesterone on Estrogen-Induced Phasic LH and Prolactin Secretion Correlated with Estrogen Nuclear and Progestin Cytosol Receptor Concentrations in Brain and Pituitary Gland

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Abstract
The purpose of these studies was to determine the temporal requirements and time of day required for progesterone (P4) to amplify versus extinguish LH surges. The experimental animal model used in these studies was the 7-day ovariectomized rat (day 0) treated continuously with estradiol (E2) for 2–4 days (days 2, 3 or 4). In these studies we also examined the changes which occur in estrogen nuclear (ERn) and progestin cytosol (PRc) receptor concentrations in the preoptic area (POA), medial basal hypothalamus (MBH), corticomedial amygdala (CMA) and pituitary gland (PIT) associated with these physiological responses. When two P4 capsules (50 mg/ml) were placed subcutaneously at 09.00 h on day 2 and removed 3 h later (12.00 h), LH surges were amplified that afternoon. 24 and 48 h later (days 3, 4) phasic LH release reoccurred albeit in reduced concentrations compared to the LH values obtained in E2-treated rats on day 2. In contrast, if P4 capsules remained in situ for < 24 h, LH surges did not reappear on day 3. In a separate group of E2-treated rats, P4 capsules were placed subcutaneously at 15.00 h and removed at 21.00 h on day 2. Only minor increases in LH occurred on day 3 compared to E2-treated controls. Thus, both the duration of time and hour of day that the hypothalamo-pituitary unit is exposed to P4 seem important in determining which component of the biphasic LH response (amplification vs. inhibition) will occur. When ERn and PRc concentrations were measured, neither 3 nor 24 h of P4 exposure affected ERn levels in the POA, MBH, CMA or PIT. However, 3 h of P4 exposure significantly reduced PRc concentrations in POA, MBH and PIT at 15.00 h on day 2, but by day 3, PRc values returned to the control levels observed in rats receiving only E2 on days 2 and 3. Continuous P4 exposure not only significantly decreased PRc levels in POA, MBH and PIT by 15.00 h on day 2, but these receptor levels still were depressed in MBH and PIT at 15.00 h on day 3. Since PRc concentrations recovered in rats exposed to only 3 h of P4 on day 2 we next examined whether P4, given at 09.00 h on days 3 or 4, would affect afternoon LH surges on these days. Both amplification and advancement of the time of LH surges occurred in these rats. Thus, with the restoration of control PRc levels in day-3 rats briefly exposed to P4 on day 2, physiological competence to respond positively to P4 is also reestablished. The final series of studies examined the effects of P4 on the PRL surges which occur concomitant with phasic LH release. Regardless of the effect of P4 on LH release, this steroid had no effect on phasic PRL release on days 2–4. We recognize that a critical time period exists during which estrogen is required to program those neural processes involved in phasic LH release the following day. Presentation of a P4 stimulus during this interval seems to disrupt some critical estrogen-dependent biochemical events in hypothalamic neurons such that phasic LH release is extinguished the next day.

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