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Neuroendocrine Actions Of Neuropeptide Y

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Neuropeptide Y and Related Peptides

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 162))

Abstract

In the two decades since its discovery neuropeptide Y (NPY) has emerged as a major peptidergic neuromessenger in neuroendocrine regulation, affecting the secretion of every anterior and posterior pituitary hormone. Innervation of these neuroendocrine networks derives from the major NPY cell group in the hypothalamic arcuate nucleus and from noradrenergic and adrenergic cells in the lower brainstem, in which NPY serves a cotransmitter role. Regarding the magnocellular neuroendocrine system, NPY directly innervates vasopressin (VP)-secreting, and probably, oxytocin (OT)-secreting, cells, and stimulates the release of both peptides. Whether such effects are important for the release of OT or VP in response to specific physiological stimuli remains to be determined, however. Much more information is available regarding NPY effects on anterior pituitary hormone secretion. NPY, mainly deriving from arcuate neurons, inhibits the secretion of prolactin (PRL), thyroid stimulating hormone (TSH) and growth hormone (GH), and stimulates the secretion of adrenocorticotropic hormone (ACTH). For the most part, these effects are exerted by altering the neurosecretion of the cognate hypothalamic releasing and/or inhibiting hormone systems that regulate anterior pituitary secretion. In addition, an action at the anterior pituitary gland is important in the NPY inhibition of PRL secretion. In the case of PRL, TSH, and ACTH, the agouti-related peptide, which is coexpressed in arcuate NPY neurons, exerts the same effect as NPY, suggesting a postjunctional co-action of these two messengers. When considered together with the critical orexigenic effects of NPY, it is evident that the arcuate NPY system is important in integrating a variety of physiological, neuroendocrine and behavioral responses to conditions of nutritional inadequacy. Moreover, changes in circulating leptin, signaling the status of adipose tissue energy stores, appears to be a major factor in orchestrating these behavioral and neuroendocrine changes via its effects on hypothalamic NPY synthesis and release.

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Crowley, W.R. (2004). Neuroendocrine Actions Of Neuropeptide Y. In: Michel, M.C. (eds) Neuropeptide Y and Related Peptides. Handbook of Experimental Pharmacology, vol 162. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18764-3_7

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