This study determined the effects of prolactin on pituitary responsiveness to LHRH in the rat. Blood samples were collected before and after treatment with LHRH. Administration of exogenous prolactin on Days 10 and 11 postpartum to females nursing two pups had no effect on basal LH or FSH secretion Day 11 or on the LH or FSH responses after LHRH administration. Whereas ovariectomy on Day 10 resulted in a significant increase in LH secretion on Day 11, administration of exogenous prolactin to ovariectomized lactating females significantly decreased the postcastration rise in LH without having an effect on the LH response to LHRH. The effect of endogenous prolactin secretion was studied on Day 10 postpartum in females nursing eight pups by inhibiting suckling-induced prolactin with bromo-cryptine for 24 hr before LHRH administration. The LH response after LHRH was similar in the presence or absence of elevated levels of prolactin. However, if the pups were removed for 24 hr before administration of LHRH, both basal LH secretion and the response after LHRH increased to levels observed during diestrus of the estrous cycle. The effect of endogenous prolactin secretion on the postcastration rise in LH and FSH was studied on Day 8 or 17 postpartum (5 days after ovariectomy) in females nursing eight pups. The results showed that whereas suckling plus endogenous prolactin secretion almost completely blocked any postcastration rise in LH or FSH, suppression of prolactin in the presence of suckling led to a very large increase in LH and FSH. In spite of large differences in the basal rate of LH and FSH secretion, LHRH-induced LH secretion was similar in the presence or absence of prolactin. These results indicate that in intact lactating females, prolactin has no effect acutely to suppress the basal rate of gonadotropin secretion or LHRH-induced gonadotropin secretion. In ovariectomized lactating females, the elevated levels of prolactin associated with lactation suppress gonadotropin secretion but do not appear to be acting at the level of the pituitary to decrease responsiveness to LHRH, and therefore must be acting at the level of the hypothalamus.
|Original language||English (US)|
|Number of pages||10|
|Journal||Biology of reproduction|
|State||Published - Dec 1 1981|
ASJC Scopus subject areas
- Reproductive Medicine
- Cell Biology