Localization of a “Feeding Center” in the Hypothalamus of the Rat

Abstract

Development of obesity in animals following destructive lesions placed in or ventrolateral to the ventromedial nucleus of the hypothalamus is a well-established fact( 1 , 2 , 3 , 4 , 5 , 6 ). This obesity has been shown to arise primarily from a marked increase in food intake, or from what has been termed “hyperphagia.” In an experimental investigation being carried out to discover the effect on food intake, etc. of small electrolytic lesions placed by the Horsley-Clarke instrument in other areas of the hypothalamus of the albino rat, a well-localized area has been found in the lateral hypothalamus, bilateral destruction of which is followed by a complete absence of eating. This area is situated in the extreme lateral portion of the lateral hypothalamus at the same rostro-caudal level (coordinate) as the ventromedial nucleus (Fig. 1). Small, bilateral, electrolytic lesions produced in this area by a current of 1 milliampere used for 15 sec, completely inhibit food intake to the point where the rat dies of starvation. On the other hand, after a unilateral lesion in this area, the animal goes on eating normally; when another unilateral lesion is made in the corresponding area of the opposite side, however, the animal then ceases to eat. This area is so well circumscribed that if the destructive lesion is placed even 0.5 to 1 mm away from it in any direction, this complete absence of eating does not develop. Bilateral lesions made in adjacent areas may result in either decreased eating or failure to eat for the first few days after the operation, but such animals resume eating within a short period.