The laryngeal chemoreflex (LCR), elicited by a drop of water in the larynx, is exaggerated by mild hyperthermia (body temperature = 40-41 deg. C.) in neonatal piglets. We tested the hypothesis that thermal prolongation of the LCR results from heating the nucleus of the solitary tract (NTS), where laryngeal afferents first form synapses in the brainstem. Three- to 13-day-old piglets were decerebrated and vagotomized and studied without anesthesia while paralyzed and ventilated. Phrenic nerve activity and rectal temperature were recorded. A thermode was placed in the medulla, and the brain tissue temperature was recorded with a thermistor approximately 1 mm. from the tip of the thermode. When the thermode was inserted into the brainstem, respiratory activity was arrested or greatly distorted in 8 animals. However, the thermode was inserted in 9 animals without disrupting respiratory activity, and in these animals, warming the medullary thermode (thermistor temperature = 40-41 deg. C.) while holding rectal temperature constant reversibly exaggerated the LCR. The caudal raphe was warmed focally by ~2 deg. C in 4 additional animals; this did not alter the duration of the LCR in these animals. Thermodes placed in the NTS did not disrupt respiratory activity, but did prolong the LCR when warmed. Thermodes that where deep to the NTS in the region of the nucleus ambiguous disrupted respiratory activity, which precluded any analysis of the LCR. We conclude that prolongation of the laryngeal chemoreflex by whole body hyperthermia originates from the elevation of brain tissue temperature within in the NTS.