The aim of this study was to evaluate neural changes in oxidative metabolism in amygdaloid sub-nuclei following unilateral electrolytic lesions of lateral hypothalamic sites that supported brain stimulation reward. A histochemical analysis of cytochrome oxidase activity, comparing lesioned to non-lesioned sides in the amygdala, revealed a significant reduction of oxidative metabolism in the cortical nucleus and, to a lesser degree, in the adjacent piriform cortex; this effect was observed 2-4 weeks after the lesion, with complete recovery by the eighth week in the case of the cortical nucleus only. No particular pattern in cytochrome oxidase activity was detected in other amygdaloid sub-nuclei that were examined, including the basolateral and medial nucleus. Within both structures, the most pronounced decreases in metabolic activity were observed at roughly the same level, corresponding to the posterolateral and posteromedial levels of the cortical nucleus and just anterior to the amygdalopiriform transition. These results suggest that within the amygdaloid complex, the cortical sub-nuclei and possibly the neighbouring piriform cortex contribute more to modulating lateral hypothalamic self-stimulation than components of the central extended amygdala.