Previous studies have shown that very low dose infusions of leptin into the 3^rd or the 4^th ventricle alone have little effect on energy balance, but simultaneous low dose infusions cause rapid weight loss and increased phosphorylation of STAT3 (pSTAT3) in hypothalamic sites that express leptin receptors. Other studies show that injecting high doses leptin into the 4^th ventricle inhibits food intake and weight gain. Therefore, we tested whether 4^th ventricle leptin infusions that cause weight loss are associated with increased leptin signaling in the hypothalamus. In a dose response study 14 day infusions of increasing doses of leptin showed significant hypophagia, weight loss and increased hypothalamic pSTAT3 in rats receiving at least 0.9 μg leptin/day. In a second study 0.6 μg leptin/day transiently inhibited food intake and reduced carcass fat, but had no significant effect on energy expenditure. In a final study we identified the localization of STAT3 activation in the hypothalamus of rats receiving 0, 0.3 or 1.2 μg leptin/day. The high dose of leptin, which caused weight loss in the first experiment, increased pSTAT3 in the ventromedial, dorsomedial and arcuate nuclei of the hypothalamus. The low dose which increased brown fat UCP 1, but did not affect body composition in the first experiment, had little effect on hypothalamic pSTAT3. We propose that hindbrain leptin increases the precision of control of energy balance by lowering the threshold for leptin signaling in the forebrain. Further studies are needed to directly test this hypothesis.