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Activity-based anorexia (ABA) in an animal model of anorexia nervosa, in which rats are allowed free access to running wheels but only 2 h food access per day. Rats exposed to this paradigm display symptoms similar to those seen in anorexic women. These include decreased food intake, increased activity, rapid body weight loss, and estrous cycle disruptions. Despite that anorexia nervosa is more frequent in women than in men, ABA has been studied almost exclusively in male rats. In Experiment 1, development of, and recovery from, ABA was characterized in female rats with and without access to running wheels. Food intake, wheel running, body weight and phase of the estrous cycle were monitored daily prior to, during, and after a period of restricted feeding in which access to food was limited to 2 h/day. This study confirmed that access to wheels is necessary for the development of ABA in female rats, and that pre-adaptation to the wheels may accelerate the weight loss associated with ABA. Following food restriction, recovery of body weight was closely associated with resumption of estrous cycles. Despite pronounced hyperphagia during the recovery phase, rats displayed estrous-related decreases in food intake. These findings suggest that satiogenic signals that decrease food intake during estrus override the orexigenic signals that stimulate appetite following weight loss. Studies in humans suggest that the serotonergic system is involved in the etiology of anorexia nervosa. In Experiment 2, the effects of fenfluramine, a serotonin agonist, on the development of ABA was examined in female rats. Food intake, wheel running, body weight and phase of the estrous cycle were monitored daily prior to, during, and after a period of restricted feeding in which access to food was limited to 2 h/day. During the restricted feeding period, rats were i.p. injected with 0.50 mg/kg fenfluramine or saline daily. In addition, development of ABA in a saline-injected group that was pair-fed to the fenfluramine-injected group was examined. Fenfluramine treatment increased the development of ABA; rats treated with fenfluramine lost weight more rapidly, and displayed greater disruptions in estrous cyclicity, than control rats. Interestingly, a reduction in food intake, similar to that observed in fenfluramine-treated rats, failed to increase the development of ABA in pair-fed rats. This finding suggests that elevated serotonergic activity, rather than a suppression of food intake, is the critical factor that increased the development of ABA in this experiment. The mechanism underlying this effect is unknown; however, it is possible that the serotonergic system interacts with other systems involved in the control of food intake, such as neuropeptide Y(NPY), to increase susceptibility to ABA. Further research is necessary to determine how hypothalamic NPY concentration changes in response to fenfluramine treatment in rats with ABA.