Cognitive impairment and gene expression alterations in a rodent model of binge eating disorder

• DOI: 10.1016/j.physbeh.2017.08.004
• Publication Date: 2017-08-15T15:31:08Z
• Authors: Anjali Chawla; Zachary A. Cordner; Gretha Boersma; Timothy H. Moran
• Keywords: Male; 0301 basic medicine; Analysis of Variance; Receptors, Dopamine D2; Brain-Derived Neurotrophic Factor; Body Weight; Brain; Receptor, Insulin; Rats; 3. Good health; Fats; Rats, Sprague-Dawley; Disease Models, Animal; Eating; 03 medical and health sciences; Gene Expression Regulation; Exploratory Behavior; Receptor, Serotonin, 5-HT2C; Animals; Receptor, trkB; Cognition Disorders; Maze Learning; Binge-Eating Disorder

Binge eating disorder (BED) is defined as recurrent, distressing over-consumption of palatable food (PF) in a short time period. Clinical studies suggest that individuals with BED may have impairments in cognitive processes, executive functioning, impulse control, and decision-making, which may play a role in sustaining binge eating behavior. These clinical reports, however, are limited and often conflicting. In this study, we used a limited access rat model of binge-like behavior in order to further explore the effects of binge eating on cognition. In binge eating prone (BEP) rats, we found novel object recognition (NOR) as well as Barnes maze reversal learning (BM-RL) deficits. Aberrant gene expression of brain derived neurotrophic factor (Bdnf) and tropomyosin receptor kinase B (TrkB) in the hippocampus (HPC)-prefrontal cortex (PFC) network was observed in BEP rats. Additionally, the NOR deficits were correlated with reductions in the expression of TrkB and insulin receptor (Ir) in the CA3 region of the hippocampus. Furthermore, up-regulation of serotonin-2C (5-HT2C) receptors in the orbitoprefrontal cortex (OFC) was associated with BM-RL deficit. Finally, in the nucleus accumbens (NAc), we found decreased dopamine receptor 2 (Drd2) expression among BEP rats. Taken together, these data suggest that binge eating vegetable shortening may induce contextual and reversal learning deficits which may be mediated, at least in part, by the altered expression of genes in the CA3-OFC-NAc neural network.