The role of the amygdala in non-homeostatic eating

The motivation to eat is influenced by both internal physiological demands and by external stimuli with positive or negative associations. A conditioned stimulus (CS) associated with food can potentiate eating in sated subjects, whereas a CS associated with a negative affect can suppress eating in hungry subjects. Although the amygdala has been implicated in these behaviors, the neural mechanisms that underlie this type of non-homeostatic eating are poorly understood. To investigate the role of BLA neurons in CS+ potentiated eating and CS- lick suppression, we developed a behavioral paradigm in mice in which eating behavior could be assessed in conditions of low or high satiety and in relation to CS presentations while recording neural activity using freely-moving endoscopic calcium imaging. We found that satiety partially decreases responses to the CS+, and the neural representation of the CS+ becomes more similar to the CS-. Additionally, we tested the hypothesis that CS-evoked activity is casually involved in CS+ induced licking or CS- lick suppression by using optogenetics during this task. Silencing of BLA glutamatergic neurons labelled by NL189 prevents CS- lick suppression during low satiety and does not affect licking during the CS+. The combination of cellular imaging and optogenetics results indicates that BLA neuronal activity evoked by the CS- is critical for lick suppression, whereas CS+ activity might facilitate appetitive behavior, but this activity is not critical for cue-induced eating