Catecholamines, Opioids, and Vagal Afferents in the Nucleus of the Solitary Tract

Abstract

There is prominent nonsynaptic vesicular release of catecholamines and/or opioid peptides in the nucleus of the solitary tract (NTS), and this occurs mainly from large dense-core vesicles (LDCVs). Catecholamines and/or opioids in the NTS can modulate both cardiorespiratory and nociceptive reflexes. In addition, both noradrenergic and adrenergic neurons in this region contain endogenous opioid peptides and receive direct synaptic input from vagal afferents. The functional sites for storage and release of catecholamines and for the physiological effects of catecholamines and/or opioids in the NTS, however, are largely unknown. To identify these sites, previously characterized antipeptide antisera is used to examine the immunocytochemical localization of the vesicular monoamine transporter-2 (VMAT2), the transporter responsible for the reserpine-sensitive vesicular uptake of monoamines in neurons; the β2-adrenergic receptor (βAR), a receptor subtype implicated in the presynaptic regulation of noradrenaline release; and the μopioid receptor (μOR), the major opioid-receptor subtype involved in modulation of vagal reflexes. The results suggest that occupancy of βAR in the NTS can modulate not only the presynaptic release and postsynaptic responses of catecholaminergic neurons, but also the activity of neighboring glia. These findings, as well as the presence of βAR on glia and μOR at extrasynaptic sites on dendrites and axons, suggest that catecholamines and opioids are involved in parasynaptic transmission.