Ultrastructural localization of neuropeptide Y Y1 receptors in the rat medial nucleus tractus solitarius: relationships with neuropeptide Y or catecholamine neurons.
Academic Article
Overview
abstract
Neuropeptide Y (NPY) Y1 receptor (Y1-R) agonists influence cardiovascular regulation. These actions may involve NPY- and catecholamine-containing neurons in the medial nucleus of the solitary tract (mNTS), at the level of the area postrema. The cellular sites through which Y1-R agonists may interact with NPY and catecholamines in the mNTS, however, are not known. To determine potential sites of action for Y1-R agonists, and their relationship to NPY or catecholamines in the mNTS, we used electron microscopic immunocytochemistry for the detection of sequence-specific antipeptide antisera against Y1-R alone or in combination with antisera against NPY or the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH). Analyses were conducted in the rat mNTS, at the level of the area postrema. Y1-R was found mainly in small unmyelinated axons and axon terminals but also in some somata and dendrites as well as a small number of glia. Within axon terminals, labeling for Y1-R was often present on dense core vesicles and small synaptic vesicles as well as extrasynaptic areas of the plasmalemma. Some Y1-R-labeled terminals also contained NPY or TH, suggesting that agonists of Y1-R may influence the release of NPY or catecholamines in the mNTS. In addition, Y1-R was found in dendrites that received asymmetric excitatory-type synapses from unlabeled axon terminals. Some of these dendrites contained NPY or TH, which indicates that Y1-R may be targeted for functional activation within NPY- or catecholamine-expressing neurons in the mNTS. These results demonstrate that Y1-R is a presynaptic receptor in NPY- or catecholamine-containing axon terminals within the mNTS as well as a postsynaptic receptor on NPY- or catecholamine-containing neurons that are contacted by axon terminals that likely contain excitatory amino acid transmitters. Agonists of Y1-R in the mNTS may thus affect cardiovascular regulation by modulating NPY, catecholamine, and excitatory amino acid transmission.
