Carotid baroreflex in the rat: role of glutamate receptors in the medial subnucleus of the solitary tract.

Experiments were done in urethane-anesthetized adult male Wistar rats to investigate the role of glutamate receptors in the medial subnucleus of the solitary tract (mNTS) in mediating the carotid sinus baroreflex responses. The carotid sinus on one side was isolated from the general circulation and perfused with a warm perfusion fluid (37 degrees C; pH 7.4) saturated with 100% oxygen. The carotid sinus was then connected to an apparatus that permitted application of pressure increments (20-100 mm Hg) to stimulate specifically baroreceptors. The mNTS ipsilateral to the isolated carotid sinus was identified by microinjections (100 nL) of L-glutamate (5 mM). The stereotaxic coordinates for mNTS were: 0.5-0.6 mm rostral to the calamus scriptorius, 0.5-0.6 mm lateral to the midline, and 0.5-0.6 mm deep from the dorsal medullary surface. Microinjections of either D(-)-2-amino-7-phosphono-heptanoic acid, which is an N-methyl-D-aspartic acid (NMDA) receptor antagonist (5 mM) or 2,3-dioxo-6-nitro-1,2,3,4-tetrahydro-benzo[f]quinoxaline-7-sulfonamide disodium (a non-NMDA receptor antagonist; 2 mM) significantly attenuated the depressor responses elicited by carotid baroreceptor stimulation. Simultaneous blockade of NMDA and non-NMDA receptors in the ipsilateral mNTS completely abolished the depressor responses to carotid baroceptor stimulation. Microinjections of either (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA; 50 mM) or (RS)-alpha-cyclopropyl-4-phosphono-phenyl-glycine (CPPG; 80 mM) did not alter baroreflex responses. AIDA blocked group I and III while CPPG blocked all three groups of metabotropic glutamate receptors (mGLURs). These results suggest that ionotropic glutamate receptors, but not mGLURs, in the mNTS mediate the reflex depressor responses to carotid baroreceptor stimulation in the rat.