The effects of high levels of progesterone secretion during lactation on the control of gonadotropin secretion in the rat

This study determined whether lactation differentially affected the magnitude of estrogen-induced LH and FSH surges. The inhibitory or stimulatory effects of elevated progesterone (P) during lactation on estrogen-induced gonadotropin surges also was investigated on days 5-6, 10-11, and 15-16 postpartum. On day 2 postpartum, litters were adjusted to eight pups (lactation) or zero pups (nonlactation), ovariectomy was performed, and the animals were divided into four groups: 1) intact; 2) ovariectomized (OV); 3) OV plus a P-filled Silastic implant on day 2 (OV + chronic P); and 4) OV plus 7 mg P at 1200 h on the day of the gonadotropin surge (OV + acute P). Estrogen treatment consisted of 1 g estradiol benzoate (EB), followed 24 h later by 50 g EB. Blood samples were collected the next day, beginning at 1100 h. Therefore, EB treatment began on days 3, 8 or 13, and gonadotropin surges were observed on days 5, 10, and 15 respectively. On day 10 postpartum, LH surges in intact lactating females were much smaller than spontaneous proestrous surges. Ovariectomy greatly reduced the magnitude of the LH surge in lactating animals. Either chronic or acute P restored the magnitude of the LH surge to levels observed in intact females. In the nonlactating females, ovariectomy also reduced the size of the LH surges, whereas exposure to P, either chronically or acutely, restored the size of the LH surge to proestrous levels. Surprisingly, FSH surges were of similar magnitude in intact lactating and proestrous animals. Furthermore, in both the lactating and nonlactating animals, ovariectomy resulted in FSH surges approximately twice the size of those observed in intact animals. Exposure to P, either chronically or acutely, had little effect on further enhancing FSH secretion. Similar results were observed in lactating animals on days 5 or 15 postpartum. To determine the site of action of P in augmenting estrogen-induced LH secretion, exogenous LHRH was administered at 1500 h on day 10 at the time of the expected LH and FSH surges. Lactating or nonlactating animals received 7 mg P at 1100 h on day 10 (OV + acute P) and then Nembutal at 1300 h to block the endogenous gonadotropin surges. The results showed that acute P had no effect on LH responsiveness to LHRH to enhance the effect of EB alone. Furthermore, the LH response to LHRH appeared to be similar in OV, EB-treated lactating, or nonlactating animals and was comparable to the responsiveness observed on the afternoon of proestrus. The following conclusions can be drawn from these experiments: 1) lactation differentially affects LH and FSH secretion, decreasing EB-induced LH surges, while having no effect on FSH surges; 2) the small LH surges are not the result of the elevated levels of P during lactation; 3) lactation greatly decreases the ability of P to enhance the LH surge; 4) pituitary responsiveness to LHRH is not greatly affected by P or lactation; and 5) some substance from the ovaries acts to suppress the magnitude of the FSH surge.