Abstract

Previous studies have involved the "posterodorsal" amygdaloid area with the control of food intake and the development of obesity in rats. Within this wide region, the posterodorsal medial amygdala (MePD) has connections with specific hypothalamic nuclei that increase feeding behavior and modulate energy balance. Glutamate is the major brain excitatory neurotransmitter, remarkably enhances centrally mediated food consumption, and is abundantly found in the MePD. Here, it was studied the effects of saline (0.3 μL) and glutamate (45 nM or 45 mM/0.3 μL) directly microinjected in the MePD of adult male rats on the consumption of a three-choice (high-carbohydrate, high-protein, or high-lipid) macronutrient selective diet. The rat adaptation to the experimental procedures and its body weight gain were continuously evaluated. Control data for all groups and results following microinjections were obtained after a fasting protocol. Feeding behavior was evaluated during the subsequent 2-hr period of free access to the selective diets. Both doses of glutamate microinjected in the MePD did not lead to a higher percentage of animals consuming any of the different diets (P > 0.05), although glutamate 45 mM induced a higher consumption of the high-carbohydrate diet when compared with presurgery control values (P < 0.01). Interestingly, present data indicate that glutamate in the male MePD induces only a subtle modification in the feeding behavior and suggest that large electrolytic lesions of the "posterodorsal" amygdaloid region might have affected other regions to alter drastically meal size consumption in rats.

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