α2A‐Adrenergic receptors are present in μ‐opioid receptor containing neurons in rat medial nucleus tractus solitarius

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Abstract
Agonists of the alpha‐2A‐adrenergic‐ (α2A‐AR) and the μ‐opioid‐receptor (μOR) jointly affect autonomic functions that are also disregulated in animals undergoing withdrawal from chronic administration of the μOR agonist morphine. Cardiovascular and gastrointestinal reflexes are mediated, in part, by the medial nucleus of the solitary tract (mNTS) at caudal (cNTS) and intermediate (iNTS) subregions. Together, this evidence suggests that α2A‐AR and μOR may be colocalized within many of the same neuronal profiles in both the intermediate and caudal mNTS. In order to examine whether α2A‐AR and μOR are present within common somata, dendrites, or axon terminals in the mNTS, we used electron microscopic immunocytochemistry for the detection of antisera against each receptor at intermediate and caudal levels of this brain region. Most of the dually labeled profiles were somata and dendrites. Of all dual‐labeled profiles in the iNTS 49% were somata and were 47% dendrites, whereas in the cNTS 61% were somata and 32% were dendrites. Within dual‐labeled profiles, the intracellular distribution of α2A‐AR and μOR differed. μOR was more frequently associated with the plasmalemma, whereas α2A‐AR was often affiliated with vesicular organelles. Few axon terminals, and even fewer glia, contained both markers. We also frequently observed single‐labeled α2A‐AR glia that apposed exclusively μOR‐containing dendrites or axon terminals. These findings indicate that somata and dendrites contain functional sites for convergent μOR and α2A‐AR activation. In addition, each receptor is positioned for involvement in intercellular signaling between apposed neurons and glia. Activation of α2A‐AR on μOR‐containing somata or dendrites, or on glia apposed to μOR‐containing neurons, may help to account for the efficacy of α2A‐AR agonists in relieving some of the autonomic symptoms of opiate withdrawal. Synapse 43:208–218, 2002.