In urethan-anesthetized rats, esophageal distension evoked volume-dependent reflex contractions with phase-locked multiunit discharges in the central subnucleus of the solitary tract complex (NTSC) and the nucleus ambiguus. During blockade of solitarial, but not peripheral, muscarinic cholinoceptors, the volume-response relationship of reflex contractions was shifted rightward with a depression in pressure wave amplitude. Concurrently, premotor NTSC responses were attenuated and nucleus ambiguus activity was abolished during esophagomotor inhibition. Both NTSC discharges and reflex responses were eliminated, or strongly inhibited, during blockade of excitatory amino acid receptors (EAARs) with 6-cyano-7-nitroquinoxaline-2,3-dione, gamma-glutamylglycine or 2-amino-7-phosphonoheptanoate. In brain stem slice preparations, whole cell recordings in the NTSC region revealed fast excitatory postsynaptic potentials (EPSPS) with spikes in response to electrical stimulation of the solitary tract. Although spiking was facilitated by muscarine, EPSPS were resistant to cholinoceptor antagonists but sensitive to EAAR blockers. We conclude that esophageal vagal afferents excite ipsilateral NTSC interneurons via activation of glutamate receptors of the DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid and N-methyl-D-aspartate subtypes. Cholinergic input to the NTSC probably derives from propriobulbar sources and serves to modulate the responsiveness of reflex interneurons.