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Submitted on December 22, 2006
Accepted on April 13, 2007
Department of Physiology & Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064; Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706
* To whom correspondence should be addressed. E-mail: Janice.Urban{at}rosalindfranklin.edu.
The neuroendocrine parvocellular corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus are the main integrators of neural inputs that initiate hypothalamic-pituitary-adrenal (HPA) axis activation. Neuropeptide Y (NPY) expression is prominent within the PVN and previous reports indicate that NPY stimulates CRH mRNA levels. The purpose of these studies was to examine the participation of NPY receptors in HPA axis activation and whether neuroendocrine CRH neurons express NPY receptor immunoreactivity (ir). Infusion of 0.5 nmol NPY into the third ventricle increased plasma corticosterone levels in conscious rats, with the peak of hormone levels occurring at 30 minutes post injection. This increase was prevented by pretreatment with the Y1 receptor antagonist BIBP3226. Immunohistochemistry showed that CRH-ir neurons coexpressed Y1 receptor immunoreactivity (Y1r-ir) in the PVN and a majority of these neurons (88.8%) were neuroendocrine as determined by intraperitoneal injections of FluoroGold. Bilateral infusion of the Y1/Y5 agonist, [leu31pro34]NPY (110 pmol) into the PVN increased c-Fos and pCREB expression and elevated plasma corticosterone levels. Increased expression of c-Fos and pCREB was observed in populations of CRH/Y1r-ir cells. The current findings present a comprehensive study of NPY Y1 receptor distribution and activation with respect to CRH neurons in the PVN. The expression of NPY Y1r-ir by neuroendocrine CRH cells suggests that alterations in NPY release and subsequent activation of NPY Y1 receptors plays an important role in the regulation of the HPA.
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