Lesions which destroy the area postrema (AP) and damage the adjacent nucleus of the solitary tract (NST) produce a constellation of behavioral signs which include overingestion of highly palatable food, exaggerated drinking in response to angiotensin II, diminished feeding in response to glucoprivation and chronically reduced body weight. The diversity of these signs, as well as the anatomical complexities of the AP and adjacent NST, suggest that more than one behaviorally relevant neural population may be damaged by lesions of these areas. Injections of the neurotoxin, capsaicin, made directly into the region of the AP and adjacent NST, cause rats to overconsume highly palatable foods when these foods are available during short (30 min) presentations or when they are available continuously. The capsaicin-treated animals, unlike rats with thermal lesions of the AP and adjacent NST, do not exhibit chronically reduced body weight or overdrink in response to angiotensin II. In addition, feeding in response to glucoprivation is undiminished in capsaicin-injected rats. These results suggest that thermal damage of the AP and adjacent NST causes overingestion of preferred foods by damaging a population of capsaicin-sensitive neurons. The other manifestations of thermal lesions of the AP and adjacent NST are probably mediated by neurons which are not susceptible to capsaicin-induced damage. Since small unmyelinated sensory neurons are most sensitive to damage by capsaicin, it may be that damage to small sensory neuron projections in the AP and/or adjacent NST produces the overconsumption of palatable foods.