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Many of estradiol's behavioral effects are mediated, at least partially, via extra-nuclear estradiol signaling. Here, we investigated whether two estrogen receptor (ER) agonists, targeting ERα and G protein-coupled ER-1 (GPER-1), can promote rapid anorexigenic effects. Food intake was measured in ovariectomized (OVX) rats at 1, 2, 4, and 22h following subcutaneous (s.c.) injection of an ERα agonist (PPT; 0–200μg/kg), a GPER-1 agonist (G-1; 0–1600μg/kg), and a GPER-1 antagonist (G-36; 0–80μg/kg). To investigate possible cross-talk between ERα and GPER-1, we examined whether GPER-1 blockade affects the anorexigenic effect of PPT. Feeding was monitored in OVX rats that received s.c. injections of vehicle or 40μg/kg G-36 followed 30min later by s.c. injections of vehicle or 200μg/kg PPT. Selective activation of ERα and GPER-1 alone decreased food intake within 1h of drug treatment, and feeding remained suppressed for 22h following PPT treatment and 4h following G-1 treatment. Acute administration of G-36 alone did not suppress feeding at any time point. Blockade of GPER-1 attenuated PPT's rapid (within 1h) anorexigenic effect, but did not modulate PPT's ability to suppress food intake at 2, 4 and 22h. These findings demonstrate that selective activation of ERα produces a rapid (within 1h) decrease in food intake that is best explained by a non-genomic signaling pathway and thus implicates the involvement of extra-nuclear ERα. Our findings also provide evidence that activation of GPER-1 is both sufficient to suppress feeding and necessary for PPT's rapid anorexigenic effect.Activation of ERα produces a rapid (within 1h) decrease in food intake that persists for 22h.Activation of GPER-1 produces a rapid (within 1h) decrease in food intake that persists for 4h.Blockade of GPER-1 attenuates the ERα-dependent decrease in 1-h, but not 4- or 22-h, food intake.Selective activation of ERα and GPER-1 is sufficient to rapidly decrease food intake in OVX rats.