抄録
The role of the hypothalamus in the eating act and the regulation of food intake has recently been established in experimental animals by stimulation and destruction of the structure. The hyperphagia with obesity and the aphagia produced by the hypothalamic lesions indicates the localization of two regulatory centers, mutually antagonistic in function, i.e. the satiety center and the feeding center. The satiety center is presumedly involved in regulation of food intake responding to the changes of visceral sensations or blood concentration of metabolic products. The destruction of the ventromedial hypothalamic region has been shown to produce hyperphagia and obesity in a variety of animals.
Apart from the study on the regulation of food intake, attempts have been made to elucidate other aspects of the eating behavior, that is, the motivation mechanism by observing the hunger-motivated behaviors or the conditioned responses. In hypothalamically hyperphagic rats, Miller et al. (1) have shown that their hunger-motivated behaviors are more easily depressed than in normal ones. In the experiments to present the possible involvement of the satiety center in the anorexigenic effect of amphetamine Epstein (2) and Reynolds (3) have found that the reduction of food intake induced by the drug is more marked in hypothalamically hyperphagic rats than in intact ones. From the observation that hypothalamically hyperphagic rats overate the dextrose-added diet, but refused to eat it when cellulose or quinine was added to the food which was still acceptable to normal rats, Teitelbaum (4) regarded them as finicky eaters. Epstein (2) suggested that this notion of finickiness might be extended to all feeding situations in the hypothalamus-lesioned hyperphagic rats.
Some pharmacological agents have been known to reduce or enchance the appetite. One of them is amphetamine, and, with other sympathomimetic drugs, it has been often used clinically in obesity control. Schmidt and Van Meter (5) observed a depressing effect of chlorpromazine on food intake in rats, and chlordiazepoxide was reported to augment the food intake and to accelerate the increase of body weight in rats and dogs (6). The clinical observations with reserpine also suggest some effects on the appetite. In the present experiment, effects of some centrally acting drugs on the hypothalamic regulatory mechanisms of feeding have been examined by observing the eating behaviors in intact and hypothalamus-lesioned rats.
