The role of estrogens is dual: they suppress basal expression of gonadotropins and enhance GnRH responsiveness at the time of the LH-surge. Estrogens are synthesized by cytochrome P450 aromatase (P450arom), encoded by the Cyp19 gene. We focused on the Cyp19 gene in rat and showed that it is expressed in gonadotropes through promoters PII and PI.f, using RT-PCR and dual fluorescence labeling with anti-P450arom and -LH antibodies. Real-time PCR quantification revealed that aromatase mRNA levels varied during the estrous cycle and were significantly increased after ovariectomy. This effect is prevented by estradiol (E2) as well as GnRH antagonist administration, suggesting that GnRH may mediate the steroid effect. Interestingly, the long-acting GnRH agonist that induces LH desensitization does not modify aromatase expression in ovariectomized rats (OVX). Administration of E2 in OVX receiving either GnRH agonist or GnRH antagonist clearly demonstrated that E2 also reduces cyp19 expression at the pituitary level. The selective ER ligand, PPT and the selective ER ligand, DPN both mimic the E2 effects. By contrast, PPT reduces LH expression while DPN does not. In addition, using transient transfection assays in a LT2 gonadotrope cell line, we provided evidence that GnRH agonist stimulated, in a dose dependant manner, cyp19 promoters PII and PI.f and that E2 decreased the GnRH-stimulation. In conclusion, our data demonstrate that GnRH is an important signal in the regulation of cyp19 in gonadotrope cells. Both common and specific intracellular factors were responsible for dissociated variations of LH and cyp19 expression.