Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Abstract

Eating disorders, such as anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorders (BED), are described as abnormal eating habits that usually involve insufficient or excessive food intake. Animal models have been developed that provide insight into certain aspects of eating disorders. Several drugs have been found efficacious in these animal models and some of them have eventually proven useful in the treatment of eating disorders. This review will cover the role of monoaminergic neurotransmitters in eating disorders and their pharmacological manipulations in animal models and humans. Dopamine, 5‐HT (serotonin) and noradrenaline in hypothalamic and striatal regions regulate food intake by affecting hunger and satiety and by affecting rewarding and motivational aspects of feeding. Reduced neurotransmission by dopamine, 5‐HT and noradrenaline and compensatory changes, at least in dopamine D2 and 5‐HT2C/2A receptors, have been related to the pathophysiology of AN in humans and animal models. Also, in disorders and animal models of BN and BED, monoaminergic neurotransmission is down‐regulated but receptor level changes are different from those seen in AN. A hypofunctional dopamine system or overactive α2‐adrenoceptors may contribute to an attenuated response to (palatable) food and result in hedonic binge eating. Evidence for the efficacy of monoaminergic treatments for AN is limited, while more support exists for the treatment of BN or BED with monoaminergic drugs. Linked Articles This article is part of a themed section on Animal Models in Psychiatry Research. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-20

Activation of Serotonin 2C Receptors in Dopamine Neurons Inhibits Binge-like Eating in Mice

“…Given that dysfunctions of brain DA system are implicated in the development of binge eating in humans (18, 19), we speculated that 5-HT 2C Rs expressed by DA neurons may be involved in the inhibitory effects of 5-HT drugs on binge-like eating. To test this possibility, we first used TPH2-CreER mice which express tamoxifen-inducible Cre recombinase exclusively in TPH2-expressing neurons.…”

“…The central dopamine (DA) system is also implicated in the pathophysiology of binge eating (18). For instance, human genetic studies have shown an increased frequency of DA transporter (DAT) and D2 receptor polymorphisms with binge pathology (19).…”

Emotional Eating, Binge Eating and Animal Models of Binge-Type Eating Disorders

“…A variety of animal models have been developed in order to characterise the possible mechanisms involved in pathological eating behaviour and weight homeostasis in humans [17][18][19][20]. These models are based upon findings from lesion studies, pharmacological manipulations and by controlling the environmental conditions of rodents.…”

“…This model involves using a gastric fistula to induce drainage of consumed food before it enters the intestine [20]. Under such states, rats show an increase in binge eating behaviour as compared to control rats [46].…”

Found in translation? Commentary on a BJP themed issue about animal models in neuropsychiatry research

“…Aberrant eating patterns are increasingly likened to addiction disorders due to common psychological and anatomical systems being implicated in both disorders. There are a number of models that recapitulate facets of both binge eating and anorexia nervosa (van Gestel et al ., ). In both cases, drugs targeting monoamine systems are a major focus of preclinical and clinical investigations.…”