Organisms eat not only in a response to signals related to energy balance. Eating also occurs in response to "extrinsic," or environmental, signals, including learned cues. Such cues can modify feeding based on motivational value acquired through association with either rewarding or aversive events. We provide evidence that a specific brain system, involving connections between basolateral amygdala and the lateral hypothalamus, is crucial for allowing learned cues (signals that were paired with food delivery when the animal was hungry) to override satiety and promote eating in sated rats. In an assessment of second-order conditioning, we also found that disconnection of this circuitry had no effect on the ability of a conditioned cue to support new learning. Knowledge about neural systems through which food-associated cues specifically control feeding behavior provides a defined model for the study of learning that may be informative for understanding mechanisms that contribute to eating disorders and more moderate forms of overeating.Key words: amygdala; hypothalamus; eating; feeding behavior; learning; goal-directed behavior; motivation Mild to severe obesity, estimated to affect ϳ60% of the adult population in developed countries, is a risk factor for a range of diseases (United States Department of Health and Human Services, 1999). Despite adverse health consequences, difficulties in achieving and maintaining weight control are common. Overeating is attributable, at least in part, to the fact that food consumption is powerfully influenced by a variety of environmental factors that are unrelated to energy requirements (Rodin, 1981;Booth, 1989). Eating can be socially facilitated (De Castro, 1997), and cues that become associated with food when hunger prevails can increase eating in satiated states (Weingarten, 1983).Recent research is beginning to define the neural systems through which such psychological processes influence eating. Under conditions that strongly potentiate feeding, laboratory rats with neurotoxic lesions of the basolateral amygdalar area (BLA) [including basolateral ("basal"), basomedial ("accessory basal"), and lateral nuclei] fail to increase eating in the presence of a conditioned stimulus (CS) that was previously paired with food (Gallagher, 2000;Holland et al., 2002). The BLA has anatomical connections with neural circuits in the hypothalamus that control feeding behavior (Elmquist et al., 1999;Swanson, 2000;DeFalco et al., 2001;Petrovich et al., 2001). It sends substantial, topographically organized projections to the lateral hypothalamic area (LHA) (Petrovich et al., 2001), which forms part of the feeding circuit and historically has been linked to initiation of feeding (Elmquist et al., 1999).The current investigation examined potentiation of feeding by a CS in rats with a preparation that disconnects the BLA and the LHA. Here we report that the BLA-LHA system is crucial for allowing learned cues to override satiety signals and stimulate eating in sated states. We further show that t...