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Neuropeptide Y activates urocortin 1 neurons in the nonpreganglionic Edinger‐Westphal nucleus
Author(s) -
Gaszner Balázs,
Korosi Anikó,
Palkovits Miklós,
Roubos Eric W.,
Kozicz Tamás
Publication year - 2006
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21177
Subject(s) - neuropeptide y receptor , urocortin , medicine , endocrinology , biology , neuropeptide , vasoactive intestinal peptide , receptor , nucleus , neuroscience
Central regulatory pathways promoting stress adaptation utilize various neurotransmitters/neuropeptides, such as urocortin 1 (Ucn1) and neuropeptide Y (NPY). Ucn1 is abundantly expressed in the nonpreganglionic Edinger‐Westphal nucleus (npEW), where it is codistributed with NPY‐immunoreactive (ir) terminals. A special role for both neuropeptides has been postulated in stress adaptation. Using double‐labeling immunohistochemistry, we observed close appositions between NPY‐ir terminals and neurons immunoreactive for Ucn1 in the rat, as well as in the human npEW. Therefore, we hypothesized that NPY might control the activity of Ucn1‐positive neurons in the npEW. To test this hypothesis, NPY was injected into the lateral cerebral ventricle of rats, resulting in a strong activation of npEW Ucn1 neurons as revealed by Fos immunohistochemistry. Ucn1 mRNA was also upregulated in the npEW 2 hours after the injection of NPY. In a search for the type of NPY receptor that mediates this NPY‐induced recruitment of npEW‐Ucn1 cells, we found that the great majority of Ucn1 cells exhibited NPY Y5 receptor immunoreactivity, and only a few of the Ucn1 cells coexpressed the Y1 receptor. We concluded that NPY, via NPY Y5 and to a lesser extent via the Y1 receptors, exerts a stimulatory action on Ucn1 cells in the npEW. Further studies are currently in progress to elucidate the significance of this NPY–Ucn1 interaction in the npEW. J. Comp. Neurol. 500:708–719, 2007. © 2006 Wiley‐Liss, Inc.