In lactating rats with large litters, the secretion of gonadotropins by the anterior hypophysis is suppressed and is not increased even after ovariectomy. This is shown by the failure of subcutaneous or intrasplenic ovarian grafts to et al., 1954) and the absence of stimulation in the ovaries of immature rats united in parabiosis with ovariectomized lactating rats (Imamichi et al., 1954). The experiments of Rothchild (1960) also revealed that follicular quiescence in the ovaries of lactating rats is due to insufficiency of gonadotropins. On the other hand, it is well established that the pars distalis autografted to extrasellar sites can no longer secrete gonadotropins, but it produces a larger amount of luteotropin than does the normal gland during the estrous cycle (Everett, 1956;Desclin, 1956;Quilligan and Rothchild, 1960). A similar situation may also be induced in rats by placing lesions in the median eminence (McCann and Friedman, 1960) or by injections of reserpine or chlorpromazine (Barraclough and Sawyer, 1959). These findings of previous workers seem to show that an increase in the secretion of luteotropin is accompanied by a reduction in the release of gonadotropins, and vice versa.In persistent-diestrous rats secured by injections of estrogen for the first 30 days of postnatal life, development of the ovaries is permanently inhibited, not only the contents of total gonadotropins (Noumura, 1958) and luteinizing hormone (Arai, 1963) of the anterior hypophysis, but also the content of luteinizing hormone releasing factor of the hypothalamus (Arai, 1963) are decidedly lower than in normal female rats. Experiments were therefore undertaken in this laboratory to ascertain whether the secretion of luteotropin is increased in such animals.Recent experiments of Kikuyama (1963) revealed that the anterior hypophysis of persistent-diestrous rats contains a much smaller amount of luteotropin than that of normal females and that corpora lutea induced in ovaries of such rats by injections of gonadotropins are not activated unless the animals are given injections of reserpine.The present paper deals with the results of further experiments showing that in persistent-diestrous rats, although no significant amount of gonadotropins is secreted, the production of luteotropin is inhibited by the central nervous system.
In Experiment 1, female rats were given a single subcutaneous injection of 1.25 mg 5alpha-dihydrotestosterone (DHT) or its propionate (DHTP) on day 5 of postnatal life. All of them showed regular estrous cycles as adults like untreated control animals. At about 60 days of age, the rats were ovariectomized and given 7 daily injections of 2 mg progesterone (P) plus 0.2 mug estradiol-17beta (ED). Uterine trauma applied on the 4th day of P-ED injections resulted in well developed deciduomata in all animals by the day after the last injection. This made a sharp contrast to the failure of female rats receiving testosterone propionate (TP) neonatally to give a positive response under similar experimental conditions (Takewaki and Ohta, 1974). The mean weight of traumatized horns was significantly larger in DHTP-treated rats (but not in DHT-treated rats) than in controls. In Experiment 2, rats were ovariectomized on day 4 and given a dose of 1.25 mg DHT or DHTP on day 5. Controls were ovariectomized on day 4 but not given any steroid on the next day. A series of 7 daily injections of 2 mg P plus 0.2 mug ED was started at about 60 days of age, after the animals had received 3 daily injections of 0.2 mug ED or 30 daily injections of 0.1 mug ED. Incidence of deciduomata following uterine traumatization was markedly lowered only in animals treated with DHTP neonatally and given 0.1 mug ED for 30 days as adults, no significant differences being found in both incidence and size of deciduomata among the other groups. It was suggested that the effects of neonatal steroid administration on uterine responsiveness in adulthood are specific to the steroid. The previous conclusion that persistent estrus in androgen-sterilized rats plays a part in the reduction of uterine responsiveness was confirmed. An exposure of rats to estrogen for a prolonged postpuberal period was without effect, unless the animals had received enough androgen neonatally.
SynopsisFemale rats were made persistent-estrous and anovulatory by giving a single injection of 1.25 mg of testosterone propionate 4 days after birth. The rats were ovariectomized when adult and given 7 daily injections of progesterone plus estradiol in amounts sufadministration of the hormones was commenced on the day following ovariectomy, or 32 or 62 postoperative days after priming with estradiol for 2 days. Incidence of deciduomata following uterine traumatization on the 4th day of the injection period was always much higher in non-androgenized controls than in androgen-sterilized rats. It seems likely that neonatal androgenization results in a permanent or at least a long-lasting reduction of uterine sensitivity to progesterone-estradiol. The longer the interval between ovariectomy and the beginning of progesterone-estradiol administration, the less marked was the mucification of the vaginal epithelium. There was no correlation between the degree of vaginal mucification and the development of deciduomata.
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