King, Bruce M., Jack T. Cook, Kirk N. Rossiter, and Bethany L. Rollins. Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport. Am J Physiol Regul Integr Comp Physiol 284: R965-R982, 2003. First published November 14, 2002 10.1152/ajpregu.00249.2002.-Small lesions centered in the posterodorsal region of the medial amygdala resulted in excessive weight gains in female rats. Unilateral lesions were nearly as effective as bilateral lesions in the first 48 h after surgery (ϩ21 to ϩ32 g). Assessment of lesion damage was done by both qualitative evaluation and by a quantitative grid-point counting method. The critical sites for weight gain were the intra-amygdaloid bed nucleus of the stria terminalis and the posterodorsal medial amygdaloid nucleus. Incidental damage to the overlying globus pallidus was negatively related to weight gain. The cupric silver method for demonstrating axonal degeneration was applied to brains with obesity-inducing lesions. A dense pattern of degenerating terminals was found in the lateral septum, amygdala, ventral striatum, and ventromedial hypothalamus. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intra-amygdaloid bed nucleus of the stria terminalis or in the posterodorsal medial amygdaloid nucleus labeled cells in the amygdala, lateral septum, and hypothalamus, reciprocating the anterograde projections from the amygdala to these areas. The data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is similar to the better-known role of this part of the brain in mediating reproductive behavior. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these two sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel. nucleus accumbens; hypothalamus; stria terminalis SEVERAL RECENT STUDIES have demonstrated that bilateral electrolytic lesions of the amygdala in female rats can result in marked hyperphagia and excessive weight gains. Daily food intake nearly doubles, and weight gains of 20-30 g during the first 3 days after lesions are not unusual (e.g., 45, 50-53, 84). Weight gains of Ն100 g in 20-25 days have been observed (50, 51). The lesions result in a marked preference for carbohydrates (53). Although food intake eventually returns to normal, the excessive weight gain is maintained indefinitely, with a marked increase in adipose tissue (50).These results are similar to those reported many years ago for cats, dogs, and primates (including humans) given amygdaloid lesions or temporal lobectomies (e.g., 9, 32, 37, 70, 103). In the rat, the effective lesion site for hyperphagia and obesity has recently been identified as the posterodorsal part of the medial amygdaloid nucleus (MePD) and the intra-amygdaloid bed nucleus of the stria terminalis (BSTIA), together ...

Lesions of the most posterodorsal aspects of the amygdala in female rats result in hyperphagia and moderate obesity. In the present study, rats with amygdaloid lesions did not increase their daily food intake when their powdered diet was diluted with 25 or 50% nonnutritive bulk. Control animals adjusted their food intake appropriately. In a second study, rats with lesions ate less food (lab chow pellets) than controls when allowed to eat for only 1 h/day for 10 days. In experiment 3, rats were offered a three-choice macronutrient diet. Whereas four of six control animals preferred the high-fat diet, all eight of the rats with amygdaloid lesions displayed a distinct preference for the high-carbohydrate diet, including those that had preferred the high-fat diet before surgery. These results, along with the previous finding that identical lesions result in hyperinsulinemia, indicate that the amygdala is involved in both the homeostatic regulation of food (caloric) intake and the selection of macronutrients.

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