alpha -2A-adrenergic receptor (alpha (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 alpha (2A)-AR-mediated actions within the mNTS have yet to be established. Immunocytochemistry was employed to examine the subcellular distribution of alpha (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 alpha (2A)-AR. The subcellular distribution of alpha (2A)-AR relative to catecholaminergic neurons also was similar within both subregions. Approximately 50% of alpha (2A)-AR-labeled somata also contained TH. In somatic profiles, alpha (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 alpha (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 neuropil at a short distance (<10 <mu>m) from alpha (2A)-AR-labeled neurons. alpha (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, alpha (2A)-AR is involved in a variety of autonomic processes, including postsynaptic modulation of mostly noncatecholaminergic dendrites, as well as influencing glia functions. J. Comp. Neurol. 433: 193-207, 2001. (C) 2001 Wiley-Liss, Inc.