Subcellular localization of α-2A-adrenergic receptors in the rat medial nucleus tractus solitarius: Regional targeting and relationship with catecholamine neurons

α-2A-adrenergic receptor (α_2A-AR) agonists modulate diverse autonomic functions. These actions are believed to involve functionally specialized, second-order neurons in catecholamine-containing portions of the medial nucleus tractus solitarius (mNTS) at both intermediate (NTSi) and caudal (NTSc) levels. However, the cellular mechanisms subserving α_2A-AR-mediated actions within the mNTS have yet to be established. Immunocytochemistry was employed to examine the subcellular distribution of α_2A-AR in both the intermediate and caudal mNTS and its association with cells containing the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). Quantitative regional comparison using immunogold showed that this receptor was distributed differentially to dendrites (NTSi, 46%; NTSc, 31%) and glia (NTSi, 29%; NTSc, 48%) at different levels of the NTS. Somata, axons, and terminals less frequently contained α_2A-AR. The subcellular distribution of α_2A-AR relative to catecholaminergic neurons also was similar within both subregions. Approximately 50% of α_2A-AR-labeled somata also contained TH. In somatic profiles, α_2A-AR labeling was often found in the cytosol and in association with endoplasmic reticulum and Golgi complexes, sites of receptor synthesis and trafficking. Approximately 20% of α_2A-AR-immunoreactive dendrites also contained TH, where the receptor was often found on extrasynaptic portions of the plasma membrane near unlabeled terminals, some of which made symmetric contacts. However, TH-labeled terminals and dendrites usually were detected in the neuropil at a short distance (<10 μm) from α_2A-AR-labeled neurons. α_2A-AR-labeled glia frequently apposed unlabeled dendrites and terminals and were often located near TH-immunoreactive dendrites. These results indicate that, within the mNTS, α_2A-AR is involved in a variety of autonomic processes, including postsynaptic modulation of mostly noncatecholaminergic dendrites, as well as influencing glia functions.