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.

Indiana University-Purdue University Indianapolis (IUPUI) / In order to elucidate the role of classical conditioning in food and alcohol co-consumption, the present study examined: (1) the effects of alcohol odor cues on alcohol and food cravings and attentional bias (bias in selective attention toward either food or alcohol pictures relative to neutral pictures); and (2) the role of alcohol odor cue elicited cravings and attentional biases on subsequent consumption. Participants (n = 77; mean age = 30.84, SD = 9.46; 51.9% female, 83.1% Caucasian) first completed the lab portion of the study. In this portion, they were exposed to alcohol and neutral odorants, after which their food and alcohol cravings and attentional bias were assessed. Participants then received an online survey the next day, on which they reported their level of food and alcohol consumption following the lab portion of the study. Using repeated measures analysis of covariance, alcohol odor cues were differentially effective in increasing food and alcohol attentional bias and cravings (Fs= 0.06 to 2.72, ps= 0.03 to 0.81). Using logistic and multiple regressions, alcohol odor cue elicited alcohol attentional bias, food attentional bias, and food cravings were associated with later alcohol consumption, but not with later food consumption or concurrent consumption (βs = -0.28 to 0.48, ps = 0.02 to 0.99; Exp(B)s = 0.95 to 1.83, ps = 0.33 to 0.91). Overall, alcohol odor cues can become conditioned stimuli that elicit conditioned food-related and alcohol-related responses, both of which persist long enough to motivate later alcohol consumption; however, these conditioned responses might not persist long enough to motivate later food or concurrent consumption. These findings serve as a first step in clarifying the role of classical conditioning in concurrent consumption. In particular, they suggest that additional empirical investigations are needed to: (1) clarify the classical conditioning mechanisms underlying concurrent consumption; and (2) examine whether interventions targeting classical conditioning mechanisms are effective for reducing alcohol use.