The Corpus Luteum-Pituitary Relationship: The Association Between the Cause of Luteotro- Phin Secretion and the Cause of Follicular Quiescence During Lactation; The Basis for a Tentative Theory of the Corpus Luteum-Pituitary Relationship in the Rat1

The regulation of pituitary luteotrophin (LTH) secretion was studied by in-vestigating a) the association between LTH secretion and follicular quiescence in lactating rats, and b) the maintenance of lactation in rats bearing denervated pituitaries. Follicular quiescence was not due to an LTH effect on the ovary, since a) exogenous LTH did not alter the mouse uterine weight response to exogenous folliculotrophins (FSH and LH; abbreviated as FTH), nor the ovarian autograft response of castrated rats to endogenous FTH, and b) pseudopregnant and lactating rats' ovaries responded to exogenous FTH as well as those of C3rcling rats. That follicular quiescence was therefore probablj' due to FTH suppression was confirmed by the following. Ovarian autografts in castrated lactators with large litters grew much less than did those of castrated post-parturient rats deprived of their litters. Castration did not increase the pituitary FTH potency of lactators nursing large litters. That FTH suppression was proportional to litter size was shown by the following. The interval to first estrus in intact lactators and in castrated lactators bearing ovarian autografts increased with the size of the litter; ovarian autotransplant growth increased with decrease in litter size. Castrates deprived of their litters and castrates nurs- ing 2-pup litters showed the same increase in pituitary FTH potency. That FTH suppression did not cause LTH secretion was shown by the following. Inj, tact and castrated lactators with small litters showed very little or no suppression of FTH, but secreted enough LTH to maintain milk secretion for normal pup growth. That LTH secretion was not continuous was shown by the facts that about 50% of rats deprived of their litters shortly after delivery became pseudopregnant, while 100% of rats suckling 1-pup litters became pseudopreg- nant (other evidence supporting the discontinuity of LTH secretion was also cited). Lactation was maintained in oxytocin-treated hypophysectomized rats bearing pituitaries autotransplanted beneath the kidney capsule; oxytocin was shown in another study not to stimulate LTH secretion. This experiment thus demonstrated that LTH secretion did not depend on stimulation from the CNS. These results appeared to support a hypothesis that a CNS influence inhibits