The following experiments were performed: (i) concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin in plasma were measured at 2, 5, 8, 10 and 15 days in female Wistar rats treated on the first day of life with 100 μg oestradiol benzoate or vehicle; (ii) females injected on day 1 with 100 μg of oestradiol benzoate or 1 mg of testosterone propionate and from day 1 to day 10 or 15 with FSH and LH were killed on day 90; (iii) females injected from day 1 to day 10 or 15 with prolactin or vehicle were killed on day 90; (iv) females injected on day 1 with oestradiol benzoate and from day 1 to day 15 with a luteinizing-hormone-releasing hormone (LHRH) agonist were killed on day 90; (v) groups of females injected on days 1, 4, 7, 10, 13 and 16 with an LHRH antagonist were killed on day 90. Onset of puberty, vaginal cycles, organ weights and hormonal plasma concentrations were measured. Females treated on the first day of life with 100 μg oestradiol showed inhibition of gonadotrophin secretion and stimulation of prolactin secretion during the neonatal period. Females injected on the first day of life with oestradiol benzoate or testosterone propionate showed, in adulthood, anovulation, ovarian atrophy, reduced FSH plasma concentrations, increased prolactin plasma concentrations and reduced pituitary prolactin content. These alterations were due neither to blocked gonadotrophin secretion nor to stimulated prolactin secretion observed immediately after steroid injection, since: (i) development of the anovulatory syndrome was not blocked by the administration of exogenous gonadotrophins or LHRH-agonist; and (ii) blockade of gonadotrophin secretion immediately after birth with an LHRH antagonist or neonatal injection of prolactin did not induce the anovulatory syndrome. It is concluded that anovulation induced by administration of neonatal steroid was mediated neither by the early inhibition of gonadotrophin secretion nor by the stimulation of prolactin secretion.