The present experiments describe the study of the metabolism of <sup>14</sup>C-arachidonic acid and the effect of exogenous norepinephrine (NE) on prostanoid production in the anterior preop-tic area and medial basal hypothalamus (APOA-MBH) of prepubertal (16 days of age) and peripubertal female rats (30 days old). Four prostanoids were produced from <sup>14</sup>C-arachidonic acid (6-keto-prostaglandin(PG)F<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and thromboxane (TX)B<sub>2)</sub> and were released to the incubating medium. The basal percent of conversion was not significantly different between them. In prepubertal rats the addition of NE (10<sup>–5</sup> M) to the medium did not modify on the synthesis of these eicosanoids. In peripubertal rats there are no significant differences in the basal production of 6-keto-PGF<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and TXB<sub>2</sub> as compared to prepubertal rats. Moreover, the percentage of conversion of arachidonic acid into the different prostanoids was similar in prepubertal and peripubertal hypothalamus. Nevertheless, when NE (10<sup>–5</sup> M) was added to the incubation medium of peripubertal hypothalamus, a significant increase in the synthesis of PGE<sub>2</sub> was observed (control: 1.75 ± 0.1; NE 2.90 ± 0.3; p < 0.01). This increase in the synthesis was not accompanied by changes in the synthesis of any of the other three prostanoids. Prazosin, a well-known α<sub>1</sub>-receptor adrenoblocker at a dose of 10<sup>-5</sup> M did not modify the production of 6-keto-PGF<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and TXB<sub>2</sub> but did induce a complete inhibition of the stimulation by NE of PGE<sub>2</sub> synthesis (NE: 2.85 ± 0.1; prazosin: 1.9 ± 0.09; p < 0.01). On the other hand, yohimbine, an α<sub>1</sub>-adrenoblocker did not modify the effect of NE on PGE<sub>2</sub> production. In summary, the results reported here demonstrated that sexual maturation involves the development of a mechanism by which NE stimulates PGE<sub>2</sub> production, an effect mediated through the α<sub>1</sub>-adrenoreceptor. The relationship of these results with the development of the positive feedback of estrogens on gonadotropin secretion during sexual maturation in the female rat is discussed.