Abstract
Binge eating is the core, maladaptive eating behavior that cuts across several major types of eating disorders. Binge eating is associated with a significant loss of control over palatable food (PF) intake, and deficits in behavioral control mechanisms, subserved by the prefrontal cortex (PFC), may underlie binge eating. Few studies, to date, have examined whether the PFC is directly involved in the expression of binge eating. As such, the present study investigated the functional role of the medial PFC (mPFC) in PF consumption, using an individual differences rat model of binge eating proneness. Here, we tested the hypothesis that binge eating proneness (i.e., high levels of PF consumption) is associated with reduced mPFC-mediated behavioral control over PF intake. In experiment 1, we quantified PF-induced Fos expression in both excitatory and inhibitory neurons within the mPFC in binge eating prone (BEP) and binge eating resistant (BER) female rats. In experiment 2, we pharmacologically inactivated the mPFC of BEP and BER female rats, just prior to PF exposure, and subsequently quantified PF intake and scores of feeding behavior. While most Fos-expressing neurons of the mPFC in both BEPs and BERs were of the excitatory phenotype, fewer excitatory neurons were engaged by PF in BEPs than in BERs. Moreover, pharmacological inactivation of the mPFC led to a significant increase in PF intake in both BEPs and BERs, but the rise in PF consumption was stronger in BEPs than in BERs. Thus, these data suggest that lower, PF-induced excitatory tone in the mPFC of BEP rats may lead to a weaker, mPFC-mediated behavioral “brake” over excessive PF intake.
Highlights
Binge eating, defined as the consumption of a large amount of food, in a short period of time, is the core, maladaptive eating behavior that cuts across nearly every major type of eating disorder (ED) that predominantly affects women (Hudson et al, 2010)
Proportions of Fos-Expressing Neurons Co-localized With Excitatory and Inhibitory Neuron Markers Overall, binge eating prone (BEP) and binge eating resistant (BER) did not differ in the proportions of all Fos+ neurons that were of the excitatory phenotype (i.e., Satb2+) or of the inhibitory phenotype (i.e., PV+, vasoactive intestinal peptide (VIP)+, or SOM+) in any brain region (Figure 1 and Table 3)
Regardless of binge eating phenotype, a majority of all Fos+ neurons were of the excitatory neuron phenotype (i.e., Satb2+, ∼85% in both BEPs and BERs), and much smaller proportions of Fos+ neurons were of the inhibitory neuron phenotype; on average, 2.2% were PV+, 14.6% were SOM+, and 1.6% were VIP+ across BEPs and BERs
Summary
Binge eating, defined as the consumption of a large amount of food (typically palatable food, PF), in a short period of time, is the core, maladaptive eating behavior that cuts across nearly every major type of eating disorder (ED) that predominantly affects women (Hudson et al, 2010). Ventromedial PFC activation is lower in women with BED during the Stroop color-word interference task as compared to their non-BED counterparts (Balodis et al, 2013), and self-reported levels of dietary restraint (e.g., reported efforts to control food intake) negatively correlate with the magnitude of PFC activation during task performance in the BED group. Combined, these data suggest that the striking abnormalities in eating behavior inherent to binge eating may be driven by deficient, PFC-mediated control over food intake
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