Estradiol exerts many of its actions by coupling with two nuclear estrogen receptor (ER) proteins, ERα, and ERβ.While the acute, anorexigenic effect of estradiol appears to involve such a mechanism, the relative contributions of ERα and ERβ are equivocal. To address this problem, food intake was monitored in ovariectomized (OVX) rats following acute administration of a selective ERα agonist (4,4′,4′′-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol, PPT; dose range = 0–200 μg), a selective ERβ agonist (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN; dose range = 0–600 μg), and a physiological (4 μg) dose of estradiol benzoate (EB). While PPT-treated rats displayed dose-dependent decreases in daily food intake and body weight, neither of these measures was influenced by any dose of DPN. In addition, DPN failed to modulate the anorexigenic effect of PPT when the two ER agonists were coadministered. Meal pattern analysis revealed that the anorexigenic effect of 75 μg PPT (a dose of PPT that produced a similar decrease in daily food intake as 4 μg EB) was mediated by a decrease in meal size, not meal number. Thus, PPT, like EB and endogenous estradiol, decreases food intake by selectively affecting the controls of meal size. The finding that acute administration of 75 μg PPT failed to induce a conditioned taste aversion suggests that the anorexigenic effect of this dose of PPT is not secondary to malaise. Taken together, our findings demonstrate that selective activation of ERα decreases food intake, body weight, and meal size in the ovariectomized rat.