Abstract
Binge eating (BE) is a maladaptive repetitive feeding behavior present across nearly all eating disorder diagnoses. BE is associated with poor psychosocial outcomes (e.g., suicidal ideation) and increased risk for obesity. Despite the substantial negative impact of BE, its underlying neural mechanisms are largely unknown. Many other repetitive behavior disorders (e.g., obsessive compulsive disorder) show dysfunction within corticostriatal circuitry. Additionally, previous pre-clinical and clinical work has highlighted an imbalance between goal-directed and habitual responding in BE. The aim of the current study was to longitudinally examine in vivo neural activity within corticostriatal regions associated with habitual behavior– the infralimbic cortex (IL) and dorsolateral striatum (DLS)– in a robust pre-clinical model for BE. Female C57BL/6 mice (N = 32) were randomized to receive: 1) intermittent (daily, 2-hour) binge-like access to palatable food (BE mice), or 2) continuous, non-intermittent (24-hour) access to palatable food (non-BE mice). In vivo calcium imaging was performed via fiber photometry at the baseline timepoint and after 4 weeks (chronic timepoint) of engagement in the model for BE. Feeding behaviors (feeding bout onset, offset) during the recordings were captured using contact lickometers which generated TTL outputs for precise alignment of BE behavior to neural data. Results in the IL showed no specific changes in neural activity related to BE. However, BE animals showed decreased DLS activity from the baseline to chronic timepoint at feeding onset and offset. Additionally, BE mice had significantly lower DLS activity at feeding onset and offset during the chronic time point compared to non-BE mice. These results point to a role for DLS hypofunction in chronic BE, highlighting a potential target for future treatment intervention.
Competing Interest Statement
The authors have declared no competing interest.
