Dependence of Mammary Stimulation upon Ovarian Tissue in Gold Thioglucose-treated Mice

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Abstract
Forty-four ovariectomized BALB/c mice received bilateral intra-ocular ovarian isografts; 34 of these were given 1.2 mg/g body weight of gold thioglucose (GTG). At biopsy 20 weeks later, mammary glands were virginal in all untreated and in 20 treated (GTG-neg.) mice. The other 14 treated animals had lactational develop?ment (GTG-pos.); these alone had shown prolonged phases of luteal function in their grafts. Many treated mice showed adiposity, but this was independent of the lactogenic-luteotropic response. Grafts were removed from approximately half of the GTG-pos. mice. At autopsy, 32 weeks after grafting, such mice had no lactation, atrophic uteri, perimedullary adrenal degeneration and persistent vaginal anestrus; their mean weight had fallen to the control level. GTG-pos. mice with grafts showed increased lactogenesis, uterine cystic hyperplasia, perimedullary adrenal degeneration, and persistent metestrus with acyclic ovarian grafts; their mean weight had been maintained. At the same time, over half of the GTG-neg. mice now showed the same mammary, uterine, adrenal, vaginal and ovarian state; over half the untreated mice were similar, except that the lactogenic response was less and the adrenal lesions almost absent. It appears that GTG may damage hypothalamic centers controlling luteotropin release, independently of those regulating appetite, thus producing luteotropic-lactogenic effects. These, and weight maintenance, appear to depend upon the presence of ovarian tissue. Ultimately, a syndrome of uterine, adrenal, vaginal, and ovarian abnormality develops. However, both this and lactogenesis may eventually appear in untreated but grafted mice; presumably ovarian grafts can effect a pituitary or hypothalamic derangement independently.