Chronic exposure to intermittent hypoxia (CIH) in animals mimics the arterial hypoxemia that accompanies sleep apnea. Humans with sleep apnea and animals exposed to CIH have elevated blood pressures and augmented sympathetic nervous system responses to acute exposures to hypoxia. Arterial chemoreceptor afferent fibers terminate within the nucleus of the solitary tract (NTS). To test the hypothesis that exposure to CIH alters NTS neurons that integrate arterial chemoreceptor afferent inputs, we examined the responses of NTS neurons to activation of AMPA and NMDA receptors following exposure to CIH. NTS neurons receiving carotid body afferent inputs were identified by placing the anterograde tracer DiA onto the carotid body 1 week before exposure to CIH. AMPA and NMDA receptor-evoked whole cell currents were measured in enzymatically dispersed NTS neurons from normoxic (NORM) and CIH rats exposed to alternating cycles of 3 min at 10% O2 followed by 3 min at 21% O2 between 8 am and 4 pm for 7 days. AMPA dose-response curves had similar EC50 but maximal responses increased in neurons isolated from DiA-labeled CIH (20.1±.8 µM, n=9) compared to NORM (6.0±.3 µM, n=8) rats. NMDA dose-response curves also had similar EC50 but maximal responses decreased in CIH (8.4±.4 µM, n=8) compared to NORM (19.4±.6 µM, n=9) rats. These results suggest reciprocal changes in the number and/or conductance characteristics of AMPA and NMDA receptors. Enhanced responses to AMPA receptor activation could contribute to enhanced chemoreflex responses observed in animals exposed to CIH and humans with sleep apnea.