α-Methyl-p-tyrosine (α-MT), a competitive inhibitor of tyrosine hydroxylase, was used to block the synthesis of hypothalamic catecholamines in immature female rats of 14, 16 and 30 days of age and in castrated adults. The administration of α-MT (300 mg/kg body weight, free base) induced a significant decay in the hypothalamic content of norepinephrine (NE) and dopamine (DA) within the first 120 min. A second dose (150 mg/kg body weight), given 2 h after the first injection, did not further modify the low catecholamine levels observed 120 min after the first α-MT administration. The administration of 300 mg/kg body weight of α-MT induced a significant increase in LH concentrations in rats aged 14 and 16 days. On the contrary, after an α-MT injection, a significant LH decrease was observed in 30-day-old and in adult castrated rats. α-MT also increased FSH levels in prepubertal rats of 16 days of age, but no change occurred in 30-day-old and in adult rats. The administration of estrogen-progesterone (EP) to prepubertal rats of 16 days of age induced a significant decrease in serum LH levels as well as in the serotonin (5-HT) and 5-hydroxyindole-acetic acid (5-HIAA) concentrations in the anterior-preoptic hypothalamic area (AH-POA), but not in the medial basal hypothalamus. No modifications in the catecholamine content of these hypothalamic areas were observed in this age group after EP administration. On the contrary, in 30-day-old rats, EP induced a significant LH release as well as an increase in AH-POA concentrations of 5-HT, 5-HIAA and catecholamines. These data show that, during sexual development in the female rat, (1) the effect of catecholamines on LHRH-LH secretion changes from inhibition to stimulation, and (2) the modification in the feedback effects exerted by EP on LH is also accompanied by a changing effect of the ovarian hormones on catecholaminergic and serotoninergic systems. On this basis, the possibility exists that sexual maturation and the onset of puberty in the female rat involve the development of qualitatively different mechanisms of gonadotrophin control through changes in the ovarian hormones-neurotransmitters-LHRH interrelatio