Abstract
The sympathoinhibitory component of the baroreceptor reflex prominently involves glutamatergic visceral afferents terminating in the nuclei of the solitary tract (NTS) and C1 adrenergic neurons of the rostral ventrolateral medulla (RVLM). As reviewed, we have used electron microscopic immunocytochemical dual labeling in these regions to precisely analyze (1) the cellular sites for synergistic or opposing responses attributed to activation of different receptor subtypes on single neurons and (2) interactions involving monoaminergic neurons identified by their content of neurotransmitter synthesizing enzymes, vesicular monoamine transporter, and frequent coexpression of endogenous opioid peptides. The summarized results provide important cellular substrates for N-methyl-D-aspartate (NMDA)-mediated glutamatergic transmission and activation of either serotoninergic (5-HT2A), adrenergic (alpha 2A), or mu- or delta opioid receptors within the baroreceptor reflex circuit.