- Estrogen (E2) inhibits food intake by activating estrogen receptor (ER) within the brain. We showed previously that activated hindbrain ERα, by E2 implantation, is sufficient to inhibit eating in ovariectomized (OVX) rats. To investigate that hindbrain ERα is required for estrogenic control of eating, hindbrain infusion of ICI directly to the 4th intracerebroventricular (4th icv) was performed in the current experiment. We first demonstrated the effect of E2 on food intake in our condition. Female intact Wistar rat showed clear typical decreased pattern of eating across the ovarian cycle. Cyclic estradiol benzoate (EB) treatment in OVX rats decreased food intake significantly. The results revealed that in our condition exogenous E2 mimic eating pattern in female intact rat as reported previously. We demonstrated next that the 4th icv infusion of ER antagonist, ICI, at 4nM and 8nM could attenuate the effect of EB on food intake. There was significant lower daily food intake from EB than from oil treatment in 1% DMSO 4th icv group. However, the effect of EB on food intake was compromised from both 4nM and 8nM ICI 4th icv groups. These results support previous report that central infusion of ICI could attenuate estradiol’s anorexigenic effect. Importantly, we demonstrated that across 12 days of ICI 4th icv ICI hindbrain infusion had no effect on FI. Further, there was no difference in the number of ERα immunopositive neurons from the selected hypothalamic nuclei. Taken together, we conclude that the 4th icv with ICI attenuated the exogenous estrogenic effect on food intake in female rat and that hindbrain appear to be the site required for estrogenic effect of food intake.