Testicular atrophy (TA) and decreased plasma luteinizing hormone (LH) levels were observed in the adult male rat after treatment with 500 µg of estradiol benzoate (EB) on the first day of life, while administration of 1 mg of testosterone propionate (TP) on the same day was also associated with TA but increased LH levels. TA and no changes in plasma LH levels were seen when the treatment was performed with similar doses of both steroids on day 5 of life. In no case were plasma follicle-stimulating hormone (FSH) levels altered by these treatments. No differences in basal LH and FSH levels were found in adult females after treatment with 100 µg of EB or 1 mg of TP on day 5. LH response to castration was lower in neonatally androgenized and estrogenized adult male and female rats than in their respective controls, while FSH response was scarcely modified. In conclusion, neonatal treatment with EB or TP in both sexes induced alterations in LH control mechanisms without changing those of FSH.

Androgenized, oestrogenized and control female and male rats were used to establish possible differences in the alteration of the prolactin control system. Neonatal treatment involved administration of oestradiol benzoate or testosterone propionate (TP) on days 1 and 5 to the males and on day 5 to the females. Oil-treated animals were used as controls. Plasma prolactin levels were measured in these animals during adulthood (a) before gonadectomy, performed on day 80, and 27 days after gonadectomy and (b) on the 2 days (at 10.00 and 17.00 h) after administration of a single dose of TP to gonadectomized animals. Oestrogenized rats had the highest plasma prolactin concentrations just before and after gonadectomy. Testosterone propionate increased plasma prolactin levels in all groups. This response was more notable in the female than in the male groups, and was highest in the oestrogenized animals. Temporal rhythms of the prolactin response to TP were daily, perhaps circadian, with increased levels in the afternoon compared with those in the morning. This pattern was not present in oestrogenized females and androgenized males. Results suggest (a) that oestrogens and androgens given neonatally differ in their ability to alter the prolactin control system, and (b) that females seem to be more sensitive than males to changes in hypothalamic differentiation induced by neonatal steroid treatment.

Female rats were submitted to light-darkness, to constant light on day 60 or to constant light from birth. Plasma prolactin was measured on days 80,100 and 120 in all experimental situations before ovariectomy was performed. 10 days later, a blood sample was taken and the animals were injected subcutaneously with 75 µg of estradiol benzoate. Blood was again drawn on 2 consecutive days. Results showed that: (a) prolactin levels were higher in the groups submitted to prolonged periods of constant light (60–120 days); (b) after ovariectomy prolactin levels decrease but remain higher in these same groups, and (c) constant light produced a higher prolactin response to estradiol benzoate. These data indicate that the length of exposure to constant light may be a critical factor in the development of alterations in the control of prolactin secretion.

Neonatally oestrogenized female rats showed hyperprolactinaemia (prolactin, 230 micrograms/l), normal LH levels and absence of a positive feedback effect of oestrogen on secretion of LH at 5 months of age. Bromocriptine treatment for 13 days (1 mg/kg per day) caused no changes in LH levels and prolactin levels decreased to normal values (33 micrograms/l). This decrease in prolactin concentration was not followed by the recovery of phasic LH response to oestrogens. The effectiveness of oestrogens to induce prolactin secretion was greater in the neonatally oestrogenized rats than in the control group. In both cases the effect diminished after bromocriptine treatment. These results indicate that hyperprolactinaemia is not the cause of the anovulatory state in oestrogenized rats and that neonatal treatment with oestrogens alters oestrogen--prolactin relations, probably involving dopamine.

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