Acute Food Deprivation Rapidly Modifies Valence-Coding Microcircuits in the Amygdala

Abstract

In the quest for food, we may expend effort and increase our vulnerability to potential threats. Motivation to seek food is dynamic, varying with homeostatic need. What mechanisms underlie these changes? Basolateral amygdala neurons projecting to the nucleus accumbens (BLA[->]NAc) preferentially encode positive valence, whereas those targeting the centromedial amygdala (BLA[->]CeM) preferentially encode negative valence. Longitudinal in vivo two-photon calcium imaging revealed that BLA[->]NAc neurons were more active, while BLA[->]CeM neurons were less active, following just 1 day of food deprivation. Photostimulating BLA[->]CeM neurons inhibited BLA[->]NAc neurons at baseline, but food deprivation rapidly converted this inhibition into facilitation, supporting a model wherein BLA[->]NAc excitability mediates invigorated food-seeking behavior after deprivation. Indeed, inhibiting BLA[->]NAc reduced motivation for a caloric reinforcer in food deprived animals. Taken together, negative valence overrides positive valence processing in satiety, but changing homeostatic needs alter reward value via a rapid shift in the balance between projection-defined populations of BLA neurons.