Objective: Binge eating is characterized by an overconsumption of palatable food, a natural reinforcer. Therefore, there is increased interest in the role of reward-based processes in binge eating. To date, results have been mixed across studies examining reward system responsivity and binge eating, showing both increased and decreased activation in the nucleus accumbens and other brain structures within reward pathways. One contributing factor to differences in results might be chronicity of binge eating (i.e., early vs. chronic), where the reward system is initially hyper-responsive to binge eating, but over time, the system becomes hypo-responsive to binge eating. As a result, in later stages of binge eating, more frequent or more severe levels of binge eating might be needed to achieve the same level of responsivity. Despite chronicity of illness being a plausible mechanism to explain differences in reward-related responsivity, no studies have examined duration of binge eating as a potential factor contributing to differences in responsivity over time. The current study used an animal model of binge eating to directly examine differences in brain activation in response to palatable food in the nucleus accumbens across chronicity of binge eating. Methods: 120 Sprague-Dawley female rats were exposed to intermittent, palatable food feeding tests. Binge eating prone (BEP) and binge eating resistant (BER) rats were identified using established methods, and randomly assigned to the early stage (i.e., six feeding tests) or chronic stage (i.e., 24 feeding tests) group. Fos expression, a measure of neural activation, was quantified in the nucleus accumbens and compared across the BER and BEP groups. Results: While there were no changes in palatable food intake (i.e., behavioral responsivity) found over time in BEP rats, there were changes in neural responsivity over time in BEP rats. Specifically, BEP rats had higher levels of c-Fos expression in the nucleus accumbens core and shell at the early stage of binge eating, compared to BER rats, suggesting an initial hyper-responsivity to palatable food in BEP rats. At the chronic stage, BEP rats showed significantly lower levels of c-Fos in the nucleus accumbens core and shell, suggesting a downregulation in responsivity to palatable food over time. This change was specific to BEP rats, suggesting that the downregulation is in response to long-term, consistent, high-levels of palatable food intake found in BEP rats (rather than lower levels of consistent palatable food intake found in BER rats). Discussion: These data strongly suggest that duration of binge eating leads to differences in neural function of the reward system. Furthermore, findings point to duration of binge eating as a factor contributing to inconsistent findings in past studies examining reward system functioning and binge eating. Results from the current study strongly suggest a need to control of stage of binge eating in future studies by including duration of illness as a covariate or examining different stages of binge eating as independent groups. Work should also focus on other structures (e.g., prefrontal cortex) and mechanisms (e.g., incentive motivation) in the reward system in order to understand if similar or other processes exhibit the same downregulation over time.
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