Hyperphagia produced by lateral amygdalar lesions in dogs.

In our previous papers (Fonberg 1965, 1967) the assumption was made, that the baso-lateral part of amygdala consists of an inhibitory ali-mentary center, similar to the "satiety center" in the ventroinedial hy-pothalamus. This assumption was mostly based on the results of our earlier experiments on cats (Fonberg and Delgado 1960, 1961) which showed that stimullation of the baso-lateral partion of the amygdaloid complex inhibits the food intake and performance of instrumental ali-mentary reactions. These findings were confirmed on dogs (Fon~berg 1963), and on rats (Morgane 1962). Several authors described hyperphagia after amygdalar ablation (Ful-and others). In most of the studies, however, large amygdalar lesions or total ablation was performed, and strict localization was not the problem under study or yielded controversial results. For example Wood (1958) observed an increase of food intake after lesions situated in the central nucleus. On the other ha~nd, Green et al. (1957) on the basis of reconstruction of amygdalar lesions on cats stated that the junction between lateral and basal nucleus is crucial for the hyperphagia syndrome. Our recent experiments seem to show, that performing a small circumscribed lesion is a good methold to localize the specialized functions of the amygdala. It was found that lesions situated in the dorso-medial part of amygdala produce aphagia with subsequent hypophagia (Fonberg 1966, 1968, 1969ab). However, if lesion involved also the lateral nucleus, subsequent