Abstract
Eating disorders are multifactorial conditions that can involve a combination of genetic, metabolic, environmental, and behavioral factors. Studies in humans and laboratory animals show that eating can also be regulated by factors unrelated to metabolic control. Several studies suggest a link between stress, access to highly palatable food, and eating disorders. Eating “comfort foods” in response to a negative emotional state, for example, suggests that some individuals overeat to self-medicate. Clinical data suggest that some individuals may develop addiction-like behaviors from consuming palatable foods. Based on this observation, “food addiction” has emerged as an area of intense scientific research. A growing body of evidence suggests that some aspects of food addiction, such as compulsive eating behavior, can be modeled in animals. Moreover, several areas of the brain, including various neurotransmitter systems, are involved in the reinforcement effects of both food and drugs, suggesting that natural and pharmacological stimuli activate similar neural systems. In addition, several recent studies have identified a putative connection between neural circuits activated in the seeking and intake of both palatable food and drugs. The development of well-characterized animal models will increase our understanding of the etiological factors of food addiction and will help identify the neural substrates involved in eating disorders such as compulsive overeating. Such models will facilitate the development and validation of targeted pharmacological therapies.
Highlights
Substance use disorders have been extensively studied in recent years, and several lines of evidence suggest that these disorders consist of neuroadaptative pathologies
The overconsumption of palatable foods has been shown to down-regulate dopaminergic reward circuitry through the same mechanisms that are affected in drug addiction; in humans the availability of striatal D2R dopamine receptors and DA release are reduced [71,72], leading to the hypothesis that reduced D2R expression in the striatum is a neuroadaptive response to the overconsumption of palatable food [22,74,86,87]
Our results show that food-seeking behavior in the face of harmful consequences was prevented by selective inactivation of noradrenergic transmission, suggesting that NE in the prefrontal cortex (PFC) plays a critical role in maladaptive food-related behavior
Summary
Substance use disorders have been extensively studied in recent years, and several lines of evidence suggest that these disorders consist of neuroadaptative pathologies. Addiction is the behavioral outcome of pharmacological overstimulation and the resulting usurpation of neural mechanisms of underlying reward, motivated learning, and memory [1,2] Substances such as alcohol, cocaine, and nicotine are extremely popular and central to the study of addiction and substance use disorders, interest is growing in the study of compulsive activities not currently characterized as substance use disorders. Mice [24], animal models that have reproduced this behavior indicate that adaptive food seeking/intake can be transformed into a maladaptive behavior under specific experimental conditions Based on this observation, the major goal of this paper is to review the results derived from animal models of compulsive eating behavior. An extended, detailed review of neurobiological and behavioral mechanisms common to drug and food addiction is beyond the scope of this paper, we will briefly summarize some of the most important findings from studies using animal models of drug and food addiction in order to track, whenever possible, the parallels between naturally and pharmacologically rewarding stimuli
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