Parabrachial nucleus induces suppression of baroreflex bradycardia by the release of glutamate in the rostral ventrolateral medulla of the rat

The involvement of glutamatergic neurotransmission in the rostral ventrolat eral medulla (RVLM) in the suppression of baroreflex bradycardia by the par abrachial nucleus (PBN) was investigated. Repeated electrical activation of the PEN increased the concentration of glutamate in the dialysate collecte d from the RVLM. The same stimulation also suppressed baroreflex bradycardi a in response to transient hypertension evoked by phenylephrine (5 mu g/kg, intravenously), Microinfusion of L-glutamate (10, 50 or 100 mu M) via the microdialysis probe into the RVLM dose-dependently elicited a significant i nhibition of baroreflex bradycardia that paralleled the concentration and t ime course of the PEN-elicited elevation in extracellular glutamate in the RVLM, The suppression of baroreflex bradycardia elicited by microinjection of L-glutamate (1 nmol) into the RVLM was appreciably reversed by coinjecti on of the NMDA receptor antagonist, dizocilpine (500 pmol), or the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (50 pmol). These results suggest that an increase in the extracellular concentration of glu tamate and activation of both NMDA and non-NMDA receptors in the RVLM may m ediate the suppression of baroreflex bradycardia by activation of the PEN. Copyright (C) 2000 National Science Council. ROC and S. Karger AG. Basel.