Food intake is reduced in hot ambient temperature in a variety of mammals, including man. Thus it appears that thermosensitive mechanisms control food intake in situations when a thermogenic activity, food intake, is counter-productive to the maintenance of normal body temperature. The neural substrates involved in the thermal control of food intake are poorly understood. Preliminary findings indicate that the neurotoxin, capsaicin, damages neural fibers involved in heat-induced reduction of food intake without altering the ability to maintain normothermia at elevated temperature in rats. This suggests that capsaicin acts to selectively lesion thermosensitive systems controlling food intake. Examination of functional deficits in thermoregulation and food intake reduction at elevated temperatures in rats treated systemically, and at localized central and peripheral sites with capsaicin should reveal the lesion sites responsible for the functional deficits. The specificity of capsaicin- induced damage to thermal controls of food intake at central or peripheral sites will be further examined using immunohistochemical and silverstain degeneration techniques. Finally, peptides will be applied at sites that demonstrate impairment of heat-induced reduction of food intake. This will provide a measure of the role of specific peptides in the thermal control of food intake.
