Mediation by nucleus tractus solitarii glutamatergic neurotransmission of the cardiovascular reflex evoked by distal esophageal distension.

Distention of the rat distal esophagus evokes an arterial pressor and a cardioaccelerator response that depends upon activation of a vagal afferent projection to the nucleus tractus solitarii (NTS). The present study aimed to determine in urethane-anesthetized rats if the afferent limb of this reflex (a) relays in the NTS subdivision known ro receive esophageal afferents, and (b) utilizes glutamatergic synapses. To this end, tetrodotoxin or the glutamate antagonists gamma-D-glutamyl-glycine, 6-7-dinitroquinoxaline-2,3-dione (DNQX) and 2-amino-5-phosphonovaleric acid (AP-5) were applied to the NTS extraventricular surface rostral to the obex. All four agents inhibited both components of the reflex. DNQX or AP-5 produced a similar reversible inhibition upon pressure ejection in the vagal esophageal afferent projection area. Application of tetrodotoxin to the dorsomedial medulla oblongata caudal to the area postrema (AP) was ineffective. Basal heart rate (HR) (except in the case of AP-5) and blood pressure increased upon NTS surface application of the antagonists but not after intra-NTS ejection. At corresponding dorsal NTS sites, focal excitation of solitarial neurons with glutamate evoked hypotension and cardiac slowing. At adjacent ventral sites in the NTS subnucleus centralis (NTSc) and/or its immediate vicinity, glutamate elicited an arterial pressor response that coincided with an esophageal contraction in most but not all cases. In conclusion, afferent fibers of the esophago-cardiovascular reflex (ECVR) probably (1) terminate in the vicinity of esophageal premotor neurons comprising the NTSc and (2) activate second-order neurons via glutamate receptors of both the NMDA and non-NMDA subtype.