Role of Proestrous Progesterone Secretion in Suppressing Basal Pulsatile LH Secretion during Estrus of the Estrous Cycle

Abstract

These studies examined the mechanisms responsible for the paucity of basal LH pulses during estrus. We confirmed our earlier observations that constant infusion of naloxone during estrus results in the immediate appearance of pulsatile LH secretion during estrus, consisting of LH peak heights and LH interpulse intervals that are similar to those observed during other days of the estrous cycle. We then tested whether the proestrous surge of progesterone was responsible for the suppression of pulsatile LH secretion during estrus. Three treatment regimens were used on proestrus to either block progesterone secretion (pentobarbital) or block its action (progesterone antiserum or the progesterone antagonist, RU 486). After treatment at 12.00 h on proestrus, blood samples were collected during estrus every 10 min for 4 h, and the plasma samples were analyzed for the pattern of LH secretion. Treatment with pentobarbital (35 mg/kg at 12:00 h) blocked the proestrous surges of LH and progesterone and resulted in pulsatile LH secretion during estrus. The LH interpulse interval (72 ± 7 min) was somewhat slower than that observed in the naloxone-infused animals (54 ± 8 min). Simultaneous treatment with pentobarbital and progesterone at 12:00 h on proestrus completely prevented the appearance of LH pulses during estrus. Treatment with either progesterone antiserum (0.5 ml, i.v.) or RU 486 (1 mg s.c.) resulted in the initiation of pulsatile LH secretion during estrus. In the RU 486-treated animals, LH peak heights and LH interpulse intervals were similar to those observed in naloxone-infused animals and during other days of the estrous cycle. These studies demonstrate that the suppression of pulsatile LH secretion during estrus is dependent on endogenous opioid tone. In addition, the proestrous surge of progesterone may be responsible for this suppression during estrus, since blocking progesterone secretion or blocking its action restores pulsatile LH secretion on estrus. We hypothesize that the proestrous surge of progesterone may cause an increase in endogenous opioid tone which then suppresses GnRH release and pulsatile LH secretion during estrus.

cFos Activity Identifies Recruitment of Luteinizing Hormone‐Releasing Hormone Neurons During the Ascending Phase of the Proestrous Luteinizing Hormone Surge

“…the central role of ovarian stcroids in initiation of the proestrous LH surge in the rat is clcar (9-1 1. [25][26][27][28]. Whereas there is evidence for a pituitary site of action.…”

Progesterone Receptor A (PRA) and PRB-Independent Effects of Progesterone on Gonadotropin-Releasing Hormone Release

“…The actions of P4 are critically important in the regulation of mammary gland development and ovulation as well as blastocyst implantation, epithelial cell proliferation, and contractility in the uterus (1)(2)(3). In neuroendocrine tissues, P4 regulates reproductive behaviors (4) and exerts feedback effects on pituitary gonadotropin secretions (5)(6)(7)(8)(9)(10)(11) and hypothalamic GnRH release (12)(13)(14). The latter actions include homeostatic feedback suppression of pulsatile GnRH neurosecretion (14 -17) as well as the inhibition of ovulatory GnRH and gonadotropin surges (18 -24).…”

Ovarian Steroid Regulation of Pulsatile Luteinizing Hormone Release During Early Gestation in the Rat

“…This compound has been shown in the rat to block P receptors in the hypothalamus-preoptic area (20), areas involved in the regulation of pulsatile LH secretion. RU486 has also been reported to initiate LH pulses on estrus in rats following its administration on proestrus (21), and to produce an earlier restoration of pulsatile LH secretion following pup removal from lactating rats (22), effects that were due to antagonism of the negative feedback action of P on pulsatile LH secretion. However.…”