Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Abstract

Binge eating and an increased role for palatability in determining food intake are abnormal adaptations in feeding behavior linked to eating disorders and body weight dysregulation. The present study tested the hypothesis that rats with limited access to highly preferred food would develop analogous opioid-dependent learned adaptations in feeding behavior, with associated changes in metabolism and anxiety-like behavior. For this purpose, adolescent female Wistar rats were daily food deprived (2 h) and then offered 10-min access to a feeder containing chow followed sequentially by 10-min access to a different feeder containing either chow (chow/chow; n ¼ 7) or a highly preferred, but macronutrient-comparable, sucrose-rich diet (chow/preferred; n ¼ 8). Chow/preferred-fed rats developed binge-like hyperphagia of preferred diet from the second feeder and anticipatory chow hypophagia from the first feeder with a time course suggesting associative learning. The feeding adaptations were dissociable in onset, across individuals, and in their dose-response to the opioid-receptor antagonist nalmefene, suggesting that they represent distinct palatability-motivated processes. Chow/preferred-fed rats showed increased anxiety-like behavior in relation to their propensity to binge as well as increased feed efficiency, body weight, and visceral adiposity. Chow/preferred-fed rats also had increased circulating leptin levels and decreased growth hormone and 'active' ghrelin levels. Thus, the short-term control of food intake in rats with restricted access to highly preferred foods comes to rely more on hedonic, rather than nutritional, properties of food, through associative learning mechanisms. Such rats show changes in ingestive, metabolic, endocrine, and anxiety-related measures, which resemble features of binge eating disorders or obesity.

Antagonism of Sigma-1 Receptors Blocks Compulsive-Like Eating

“…In this study, we show that daily intermittent availability of a highly palatable diet forced subjects to periods of 23 h of abstinence, inducing a progressive and dramatic escalation of operant responding for the sugary food (Corwin and Buda-Levin, 2004;Cottone et al, 2008bCottone et al, , 2009b. Indeed, Palatable rats quickly learned the time-limited availability of the preferred dietary option, and began eating significantly more than Chow rats after only the second 1-h access to the Sig-1R blockade and compulsive-like eating P Cottone et al highly palatable diet.…”

“…This procedure allowed for a fine measurement of food responding, as well as rate and regularity of intake. It was hypothesized that rats under limited access conditions to the highly palatable diet would rapidly develop binge-like eating, and would increase the rate and the regularity of intake (Corwin, 2004;Cottone et al, 2007aCottone et al, , 2007bCottone et al, , 2008b; in addition, we hypothesized that blockade of Sig-1R would revert the maladaptive behaviors. We then provided control and bingeing rats with the standard chow diet and the highly palatable diet, respectively, in a bright, aversive compartment of a light/dark conflict box, and tested the effects of the selective Sig-1R antagonist BD-1063.…”

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

“…Cottone et al [16][17][18] found that withdrawal from extended, intermittent access to palatable food increases anxiety and decreases effortbased responding for less palatable chow, an effect linked to elevated corticotrophin-releasing factor receptor-1 (CRF-R1) signalling in the amygdala. 19 HFD removal is reported to increase operant responding for sucrose rewards in obesity-prone but not obesity-resistant rats, 20 however, it is not known if withdrawal from chronic high-fat feeding increases anxiety and palatable food reward, independent of genetic factors that enhance susceptibility to weight gain and which neurobiological changes are involved.…”

The Uncompetitive N-methyl-D-Aspartate Antagonist Memantine Reduces Binge-Like Eating, Food-Seeking Behavior, and Compulsive Eating: Role of the Nucleus Accumbens Shell

“…Core diagnostic criteria for binge-eating disorder include excessive consumption of food within brief periods of time, accompanied by loss of control, uncomfortable fullness, and intense feelings of disgust and embarrassment (APA, 2013). Growing evidence suggests that binge eating may result from neuroadaptative mechanisms in discrete areas of the brain that parallel drug and alcohol addiction (Avena et al, 2008;Corwin, 2006;Cottone et al, 2008b;Micioni Di Bonaventura et al, 2014;Parylak et al, 2012).…”