Familiar Chow Research Articles

Role of conditioned taste aversion in the development of activity anorexia

Activity anorexia (AA) occurs when rats are restricted to one meal period (60–90 min) each day and have unlimited access to a running wheel the rest of the time. This AA procedure also contains the conditions necessary for conditioned taste aversion (CTA). The food eaten during the meal period is the conditioned stimulus paired with the unconditioned stimulus produced by wheel running. Thus, CTA to food may account in part for the decreased eating in AA. To test this possibility, male rats were subjected to the AA procedure. They had daily 90-min exposures to their familiar chow and spent the rest of the day in running wheels (experimental condition) or home cages (control condition). A second, concurrent experiment had the same procedure except that novel, rather than familiar, food was used. In both experiments, AA occurred; the rats allowed to wheel run ate less than those in the control condition. Several days after AA training, a two-food preference test assessed whether CTA occurred. Wheel running induced CTA when food was novel but not when it was familiar. Since AA is typically studied with procedures using familiar food, the present findings indicate that CTA plays little or no role in AA.

Transient Overconsumption of Novel Foods by Deafferentated Rats: Effects of Novel Diet Composition

We recently demonstrated that capsaicin-treated rats consume more of an unfamiliar high-fat diet than vehicle-treated controls, but only on initial exposure (Chavez et al, 1997). We hypothesized that negative feedback signals carried by capsaicin-sensitive visceral afferents are critical for the regulation of intake of novel foods, but redundant pathways take over during subsequent exposures. To examine the role of nutrient content of the novel diet, rats were systemically treated with capsaicin ( n = 15) or vehicle ( n = 10), and exposed to 1) a fat/olestra diet that was isocaloric with chow; 2) a readily accepted fat-free cake; and 3) pure corn oil. Each 3-h feeding trial was preceded by 24-h food deprivation. Treated rats did not overconsume familiar chow, but did consume 50% more than controls of both the fat/olestra diet and the corn oil on first exposure; this suggests that capsaicin eliminated visceral afferents that normally carry satiety signals. However, the effect with the fat/olestra mixture was due primarily to depressed intake by controls, unlike the pure fat diets; this apparent neophobic response was blunted in treated rats. Because treated rats failed to overconsume the fat-free cakes, the neural system damaged by capsaicin appears to be linked to energy or fat sensory mechanisms, and possibly to hedonic responsiveness.

Vagotomy produces learned food aversions in the rat.

Subdiaphragmatic vagotomy produces hypophagia and weight loss in normal rats and can reverse the hyperphagia and obesity of rats with ventromedial hypothalamic lesions. Vagotomy surgery can also produce symptoms of nausea and discomfort. Since such symptoms are highly effective as unconditioned stimuli in food aversion conditioning, the present studies examined whether some of the depression in food intake observed in rats with vagotomy could be due to the development of aversions to the foods eaten after their surgery. In the first study, significant aversions developed to the specific novel diet consumed after vagotomy, results indicating that the symptoms associated with vagotomy can serve as effective unconditioned stimuli in the acquisition of learned food aversions. The second study compared vagotomized animals consuming familiar laboratory chow with those consuming a novel diet. In contrast to the novel diets, learned aversions did not develop to the familiar chow, and hypophagia was less persistent and severe. It is concluded that learned food aversions can contribute to the appetite and weight loss exhibited by vagotomized animals. Consideration of the conditions under which these aversions arise after vagotomy surgery may allow for the design of studies so as to minimize the aversions and thereby separate these nonspecific effects from direct regulatory deficits produced by vagotomy.

Effects of benzodiazepines and naloxone on food intake and food preference in the rat

After four days of administration, chlordiazepoxide (5 mg/kg) increased the weight gain of rats on ad libitum food and water, whereas chlordiazepoxide (7·5 mg/kg) and lorazepam (0·25 and 0·5 mg/kg) decreased it. After a period of food deprivation, chlordiazepoxide (7·5 mg/kg) and lorazepam (0·5 mg/kg) increased food consumption after ½, 2 and 6 h. In a food preference test chlordiazepoxide (5 mg/kg) enhanced consumption of chocolate chips, whereas lorazepam (0·25 and 0·5 mg/kg) enhanced consumption of familiar chow. Chlordiazepoxide (5 and 7·5 mg/kg) enhanced consumption of unfamiliar chow, whether this was preferred or not, whereas lorazepam (0·25 and 0·5 mg/kg) enhanced consumption of familiar chow. Naloxone (4 mg/kg) reduced food intake in the first ½ h after injection and reduced consumption of unfamiliar chow. Naloxone (2 and 4 mg/kg) abolished consumption of chocolate chips in the food preference test.

Altered food preferences after lesions in the basolateral region of the amygdala in the rat.

Rats with lesions in the basolateral amygdala chose different foods from control rats in 10-min. food-preference tests. The normal rats ate primarily familiar chow, while the amygdala-lesioned rats ate primarily novel foods. The lesioned rats did not select indiscriminately but showed definite preferences. With repeated testing, the normal rats' preferences became similar to those of the amygdala-lesioned rats. Food-preference tests in a disturbing environment suggested that the difference between the lesioned and control groups was not due to a general alteration in behavior such as fear. Other aspects of ingestive behavior, such as body weight regulation, were not primarily altered by the lesions. The basolateral amygdala may therefore be concerned with the selection of foods on the basis of previous experience. Amygdaloid neurons are activated in eating and drinking elicited by electrical stimulation of the lateral hypothalamus in rats (E. T. Rolls, 1972). This indication that amygdaloid neurons are involved in eating and drinking is strengthened by the finding that the amygdaloid neurons directly excited by the stimulation have the same absolute refractory period as the neurons through which the eating and drinking are elicited (E. T. Rolls, 1973). To investigate further the role of the amygdala in eating, ingestive behavior following amygdaloid lesions was analyzed, as described here. The lesion electrodes were aimed at the basolateral region of the amygdala, which is the area in which neurons were activated in the electrically elicited eating and drinking (E. T. Rolls, 1972). Electrophysiological and behavioral studies (see E. T. Rolls, 1972) support the hypothesis that the amygdala is involved in reinforcement. This hypothesis was utilized in the experiments described here. A choice of foods was given to the lesioned animals to determine whether the reward value of different foods measured by food preference is altered by the lesions.