Hypothalamic-Pituitary Responsiveness during Lactation in the Rat: Estrogen-Induced Luteinizing Hormone Surges*

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Abstract
Hypothalamic-pituitary responsiveness during lactation was studied by determining the ability of estrogen to induce surges of LH [luteinizing hormone]. In intact females nursing 8 pups, 50 .mu.g estradiol benzoate (EB) on either day 4, 9, or 14 postpartum induced surges of LH the following day that were similar in magnitude, timing and duration. The results from females nursing 2 pups were similar to those from females nursing 8 pups. When compared to the proestrous surge of LH, the surges in intact lactating animals had an earlier onset and decreased peak concentration of LH. The effect of high levels of progesterone on EB-induced LH surges was determined during pregnancy, when progesterone concentrations were similar to those during lactation. On day 14 of pregnancy 50 .mu.g EB evoked LH surges the following day that did not differ from proestrous surges. During lactation the decreased ability of the hypothalamus to respond to estrogen is most likely due to the suckling stimulus or prolactin. The effects of suckling were most clearly demonstrated in the ovariectomized females nursing 8 pups. On either day 4 or 9, 50 .mu.g EB induced LH surges the following day that were significantly smaller than those in intact lactating females. By day 15, LH surges with similar peak concentrations were observed in ovariectomized and intact females. The factors responsible for the larger LH surges in intact females were studied by treating intact females nursing 8 pups with CB-154 [2-bromo-.alpha.-ergocryptine] to inhibit prolactin and, indirectly, progesterone secretion. After treatment with CB-154, EB-induced LH surges were much smaller than in control animals. Suckling, in the absence of ovarian steroids, may greatly suppress hypothalamic-pituitary responsiveness to estrogen, since this inhibitory influence of suckling is much less effective in intact lactating animals.