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

Abstract

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 (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. J. Comp. Neurol. 433:193–207, 2001.