Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with
eating disorders. Research using animal models of
eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of
binge eating,
bulimia nervosa, or
anorexia nervosa. The findings suggest that alterations in
dopamine (DA),
acetylcholine (ACh) and
opioid systems in reward-related brain areas occur in response to
binge eating of palatable foods. Moreover, animal models of
bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of
anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based
anorexia model suggests alterations in mesolimbic DA and
serotonin occur as a result of restricted eating coupled with excessive wheel running. These findings with animal models
complement data obtained through neuroimaging and
pharmacotherapy studies of clinical populations. Information on the neurochemical consequences of the behaviors associated with these
eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here. This article is part of a Special Issue entitled 'Central Control of Food Intake'.