Presence of mu-opioid receptors in targets of efferent projections from the central nucleus of the amygdala to the nucleus of the solitary tract.

Opioids acting at mu-opioid receptors (MORs) within the nucleus of the solitary tract (NTS) potently modulate autonomic functions that are also known to be influenced by inputs from the central nucleus of the amygdala (CEA). In addition, many of the physiological effects of MOR agonists have been attributed to interactions with neurons that contain gamma-aminobutyric acid (GABA), one of the neurotransmitters present in CEA-derived terminals and their targets in the medial NTS. Together, these observations suggest that MORs are present at pre- or postsynaptic sites within the CEA to NTS circuitry. To test this hypothesis, we combined anterograde transport of biotinylated dextran amine (BDA) with immunogold-silver localization of an antipeptide antiserum against the MOR in the NTS of adult rats. In animals receiving bilateral CEA injections of BDA, anterogradely labeled axons were seen throughout the rostrocaudal NTS. Electron microscopy of the medial NTS at rostral and intermediate levels showed anterograde BDA-labeling in many small unmyelinated axons and axon terminals, none of which contained detectable MOR. The BDA-labeled axon terminals formed mainly symmetric, inhibitory-type synapses with somata and dendrites. Over half of the somatic and approximately 10% of the dendritic targets showed nonsynaptic plasmalemmal immunogold labeling for MOR. The BDA-labeled axon terminals were also frequently apposed by other small axons that contained MORs. These results suggest that within the medial NTS, MOR agonists modulate the postsynaptic inhibition produced by CEA afferents and also play a role in the presynaptic release of other neurotransmitters.