There is an interaction between the reproductive axis and the energy homeostasis. One possible mediator of this interaction is the leptin, a hormone that acts in the control of metabolism, feed behavior and reproduction. Homozygous animals for the gene “ob” (ob/ob) do not produce leptin, and present obesity and infertility. These effects are reversed after systemic administration of leptin, but the gonadotropin-releasing hormone (GnRH) neurons not express the leptin receptor (Ob-R) and a trasynaptic action of leptin on GnRH neurons is more likely. On the other hand, the estrogen may modulate the secretion of leptin by adipocytes and the expression of the Ob-R. The aim of this work was verify the effect of leptin on the luteinizing hormone (LH) secretion under estrogen modulation in female rats. Methods: Wistar female rats with regular estrous cycles were anaesthetized (tribromoethanol, 250mg/kg body wt, i.p.) and received a cannula in the 3V. After two regular cycles estrous the rats received estrogen antagonist, tamoxifen subcutaneous (s.c.) (TMX, 3mg/rat), in the metestrous and diestrous. In the day of proestrous, these animals received rat leptin intracerebroventricular (i.c.v.) (0,3;1;3μg/μl) and were killed by decapitation at 5:00 pm and the blood was collected . Results: Our results showed that the injection of 3ug of leptin in the animals without TMX amplified the plasma LH concentration on the proestrous afternoon (F(3,82) = 2,64 p<0,05; Duncan p<0,05; vehicle: 28,66 +/- 7,13 ng/ml; 3μg leptin: 83,90 +/- 27,38 ng/ml). Furthermore, TMX blocked the LH secretion in the afternoon of proestrous (F(1,82) = 39,28 p<0,05; Duncan p<0,05; vehicle: 28,66 +/- 7,13 ng/ml; TMX: 4,74 +/- 0,5 ng/ml) the injection of leptin did not restore the plasma LH concentration in the animals treated with TMX. Conclusion: Our results indicate that the central action of leptin on LH secretion depends on estrogen modulation.