Adult female rats received bilateral corticomedial amygdala lesions, olfactory bulbectomy, or sham surgery. Following ovariectomy, luteinizing hormone (LH) responses to estradiol benzoate (EB) and progesterone (P) treatment were assessed. With 4 weeks separating each injection, each rat received at 1200 h each of 3 doses of EB: 0.7, 3.5 and 7.0 �sg!100 g BW. Oil or 2mg of P was administered 72 h after EB treatment. Jugular blood samples (0.5 ml) were taken 5 times for each dose of EB: 43 h prior to, and 5, 29, 53 and 77 h after EB administration. Five hours after the 0.7 pg/100 g BW dose of EB, and at both 5 and 29 h after the 3.5 �ig!10O g BW dose of EB, plasma LH levels were depressed in all groups, but subsequently recovered to near pre-EB levels. Plasma LH levels were also depressed 5 and 29 h after the 7 �g EB/100 g BW dose in all groups, but by 53 h LH levels were’signiflcantly elevated beyond pre-EB levels when analyzed without regard to surgical treatment. However, the rats with corticomedial amygdala lesions did not respond to this high dose of EB; plasma LH titers 53 h post-EB were only equivalent to pre-EB levels. Regardless of surgical treatment, all rats given P 72 h after EB treatment responded with elevated LH levels relative to LH levels in oil-treated controls. As the dose of EB increased from 0.7 to 7 Mg/100 g BW, the magnitude of the P-induced rise in LH increased. Thus, although olfactory bulbectomy was without effect, corticomedial amygdala lesions attenuated LH elevations induced by EB but not those induced by EB plus P treatment. The corticomedial amygdala may play a role specifically in the positive feedback action of EB.