Binge eating disorder (BED) is the most prevalent eating disorder. Binge episodes are characterized by the consumption of a large amount of high-calorie food in a short period, accompanied by a sense of loss of control. BED is associated with comorbidities such as obesity and mood disorders. Several studies suggest that neuroinflammation occurs in reward-related brain circuit following bingeing on food high in sugar. In addition, preclinical studies in rat highlight cognitive consequences of binge-sucrose intake, affecting both anxiety levels and memory performance, with inconsistent results. We hypothesize that molecular mechanisms altering central inflammatory processes may participate to behavioral adaptations observed following maladaptive feeding behavior. We tested this hypothesis using a model of BED in which juvenile male rats had intermittent (2h/d, 3d/week) access to 10% sucrose solution in a two-bottle choice paradigm. Bingeing behavior was assessed as significantly higher sucrose intake during the first hour of access in the intermittent, compared with a continuous, access group. Following 6 weeks of access, anxiety was assessed in the elevated plus-maze and the open field tests, and memory performance was evaluated using object and place recognition, Morris water maze, and fear conditioning tests. In a parallel cohort, differential neuroinflammatory gene expression was assessed using qPCR. Our preliminary results show gene regulations in the NF-kB pathway in the medial prefrontal cortex and ventral hippocampus, and indicate a deficit in long-term spatial memory in bingeing rats. Overall, this work contributes to characterize neurobiological mechanisms involved in BED and may lead to new therapeutic strategies.