A rat in the labyrinth of anorexia nervosa: Contributions of the activity‐based anorexia rodent model to the understanding of anorexia nervosa

Abstract

Activity-based anorexia (ABA) is an analogous animal model of anorexia nervosa where food-restricted rats develop excessive running activity when given free access to a running wheel; their body weight sharply decreases, and finally self-starvation and death ensue unless animals are removed from the experimental conditions. The parallel of this animal model with major signs in the human disorder has been the focus of much attention from researchers and clinicians as a platform for translational research. The paper reviews the historical antecedents of ABA, research characterizing its occurrence, and its main limitations and strengths as a model of AN. As a symptomatic model of AN, the ABA model can provide clinicians with innovative and alternative routes for improving the treatment of AN.

NR2A- and NR2B-NMDA receptors and drebrin within postsynaptic spines of the hippocampus correlate with hunger-evoked exercise

“…When these two environmental factors are applied simultaneously, a rat's voluntary wheel running increases dramatically (Aoki et al 2016). This food-restriction-evoked hyperactivity, termed activity-based anorexia (ABA), has been used as an animal model for AN (Guisinger 2003; Casper et al 2008; Gutierrez 2013). AN is the mental illness with the highest mortality rate, estimated to be 200 times higher than the rate of suicide in the general US population (Arcelus et al 2011; Sullivan 1995).…”

Anorexia nervosa as a motivated behavior: Relevance of anxiety, stress, fear and learning

“…In this paradigm, when food access is restricted in the presence of a running wheel, animals paradoxically increase their exercise, consume less food than sedentary controls and lose more weight, running themselves to death within a few weeks. There is individual vulnerability in susceptibility to ABA, but young female rats with higher activity levels at baseline tend to eat the least, run the most, and lose the most weight [68][69][70], consistent with the clinical observation in AN that excessive exercise often precedes dieting and escalates with weight loss [71,72]. Excessive exercise has long been recognized as a hallmark of AN [73], is present in up to 80% of cases and appears to play a central role in the pathogenesis and progression of the disorder [74].…”

Genetics and epigenetics of eating disorders

“…A significant number of these studies have used behavioral manipulations in wild type strains of rodents to produce distinct ED-related phenotypes, a topic that has been comprehensively reviewed by others. 167–169 In this section, we restrict our discussion to experiments using model organisms with either spontaneous or induced genetic variations. Globally, these studies have revealed a complex network of genes functioning within anatomically and genetically defined neuronal ensembles to regulate different modalities of feeding.…”