SUCROSE BINGEING IN MICE: CONSEQUENCES ON MOTIVATION AND BRAIN ACTIVITY

Food intake is regulated by homeostatic and hedonic mechanisms. The arcuate nucleus of the hypothalamus (ARC) integrates metabolic signals controlling energy balance, whereas the mesocorticolimbic dopaminergic system mediates hedonic feeding, particularly in response to palatable foods such as sugar and fat. The constant availability of palatable food has contributed to eating disorders characterized by impaired control over intake. Among these, binge eating disorder (BED) is the most prevalent and is defined by excessive consumption of palatable food within a short time window, leading to physical and psychological consequences. Preclinical studies using animal models of BED have reported functional alterations in reward-related brain regions, notably the ventral tegmental area (VTA), which plays a key role in motivational processes. Based on these observations, we hypothesized that neuroadaptations within the mesocorticolimbic pathway underlie altered reward processing in BED. To investigate behavioral and cellular adaptations associated with BED, we used a sucrose bingeing model based on intermittent access (4 h/day) to a 17% sucrose solution in a two-bottle choice paradigm for 8 weeks. Binge-like behavior was defined as excessive sucrose consumption during the first hour of access. Motivation for sucrose was assessed using an operant progressive ratio schedule, and neural activity was evaluated using cFos immunostaining. In male C57Bl6/J mice, sucrose bingeing did not alter motivation but induced increased neural recruitment in both the VTA and ARC. Importantly, experiments conducted in female mice revealed sex-dependent differences in motivation and brain activation, which may contribute to the higher prevalence of BED observed in women.