[Show abstract][Hide abstract] ABSTRACT: Environmental factors contribute to the motivation to eat and can override homeostatic signals to stimulate eating in sated states, or inhibit eating in states of hunger. In particular, stress, fear, and anxiety have been linked to suppression of eating and anorexia nervosa. Here, we use a rodent model of an aversive cue-induced cessation of feeding. In this setting, food-deprived rats suppress eating when presented with a tone [conditioned stimulus (CS)] that was previously paired with footshocks [unconditioned stimulus (US)]. To begin to delineate the underlying neural circuitry we examined the two regions of the amygdala with well known roles in associative learning--the central nucleus (CEA) and the basolateral area (BLA; includes the basolateral, basomedial, and lateral nuclei). We produced selective, bilateral, neurotoxic lesions of the CEA or BLA, and then trained these rats together with sham-lesioned controls in a behavioral protocol that allowed a test for food consumption in the presence of an aversive CS. Both sham- and BLA-lesioned rats showed inhibition of eating when presented with the CS. In contrast, bilateral, neurotoxic lesions of the CEA abolished this effect. These results demonstrate that the CEA, but not BLA, is critical for control of feeding by an aversive CS. Previously we demonstrated that enhancement of eating by an appetitive CS is dependent on the integrity of BLA, but not CEA. Those findings together with the current results show a double dissociation between amygdalar subsystems that control food consumption by appetitive and aversive learned cues.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 12/2009; 29(48):15205-12. DOI:10.1523/JNEUROSCI.3656-09.2009 · 6.75 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Motivation plays an important role in the control of food intake. A cue that acquires motivational properties through pairings with food consumption when an animal is hungry can override satiety and promote eating in sated rats. This phenomenon of conditioned potentiation of feeding is mediated by connections between the forebrain and the lateral hypothalamic area (LHA). In a recent study using markers for cellular activation, neurons in the ventral medial prefrontal cortex (vmPFC) that project directly to the LHA were strongly engaged after exposure to a conditioned cue that stimulates eating in sated rats. Here, we examined whether those vmPFC neurons are necessary for conditioned potentiation of eating. We trained rats in a paradigm in which the context provided conditioning cues. Rats with bilateral neurotoxic lesions of vmPFC were impaired in context-enhanced food consumption in tests when the rats were sated. At the same time, vmPFC lesions did not produce changes in food consumption in the home cage or changes in body weight during training. Thus, vmPFC neurotoxic lesions produced impairment in food consumption specifically driven by conditioned motivational cues. The current findings suggest a critical role for vmPFC in the brain network that mediates control of conditioned motivation to eat perhaps by a mechanism akin to appetite or craving.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 07/2007; 27(24):6436-41. DOI:10.1523/JNEUROSCI.5001-06.2007 · 6.75 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Explicit cues associated with food consumption when hunger prevails will enhance eating when they are subsequently presented under conditions of satiety. Here we examined whether contextual conditioned stimuli (CSs) paired with consumption of food pellets while rats were food-deprived would enhance consumption of this food in rats that were not food-deprived. The conditioning context enhanced rats' consumption of the training food, but it did not change their consumption of the familiar, lab chow. These results show that the contextual CSs, like discrete cues, could modulate food consumption in a CS-potentiated eating paradigm. Furthermore, the data suggest that CS-potentiation of eating does not induce a general motivation to eat, akin to hunger, but instead more likely produces a more specific motivational state, akin to craving.