The Relative Contribution of Suckling and Prolactin to the Inhibition of Gonadotropin Secretion during Lactation in the Rat

Abstract

The relative contribution of suckling and prolactin to the suppression of the postcastration rise in LH [luteinizing hormone] and FSH [follicle stimulating hormone] was studied. Litter sizes were adjusted to 2 or 8 pups on Day 2 postpartum. Control animals had their litters removed at the time of ovariectomy (O-pup controls). In females nursing 8 pups, ovariectomy on Day 3 postpartum did not result in any significant increase in LH or FSH secretion on Day 8. However, if prolactin secretion in the ovariectomized lactating females was inhibited with CB-154 [ergocriptine] from Days 3-8, LH secretion increased significantly, whereas FSH increased maximally to reach levels observed in O-pup controls. The simultaneous administration of ovine prolactin with CB-154 prevented the increase in LH and FSH secretion. In contrast to the complete suppression of the postcastration rise in LH and FSH observed during early lactation, lactating females ovariectomized on Day 12 postpartum showed significant increases in LH and FSH secretion on Day 17. Gonadotropin levels had increased to approximately 50% of the values observed in O-pup controls. If the ovariectomized lactating females were treated with ovine prolactin from Days 12-17 postpartum, the postcastration rise in LH and FSH was completely suppressed. Surpisingly, administration of prolactin to the O-pup controls had no Inhibition of prolactin secretion with CB-154 resulted in maximum postcastration increases in LH and FSH in spite of the presence of suckling. The ability of prolactin to suppress the postcastration rise in gonadotropin secretion was then studied in females nursing 2 pups. After ovariectomy on either Day 4 or 11 postpartum, the increases in LH and FSH observed 1 or 2 days later were similar whether 2 pups or O pups suckled. Neither administration of prolactin nor increasing the litter size from 2-8 pups at the time of ovariectomy on Day 4 had any effect on the postcastration increase in gonadotropin secretion. However, these treatment regimens caused a significant decrease in the postcastration rise in LH and FSH on Days 12 and 13 postpartum. Again, administration of prolactin was ineffective in suppressing gonadotropin secretion in O-pup controls. Prolactin can suppress the postcastration rise in gonadotropin secretion. During early lactation, the suckling stimulus contributes more than prolactin to the suppression of the postcastration rise in LH, whereas the elevated levels of prolactin account for the suppression of FSH secretion. During the latter part of lactation, as the suppressive effects of the suckling stimulus wane, prolactin alone accounts for the decrease in gonadotropin secretion. However, the presence of the suckling stimulus appears to be necessary for the inhibitory effects of prolactin to be manifested.