Vascular neuropeptide Y Y1-receptors in the rat kidney: vasoconstrictor effects and expression of Y1-receptor mRNA

Neuropeptides ◽  
1999 ◽  
Vol 33 (4) ◽  
pp. 253-259 ◽  
Author(s):  
A. Modin ◽  
R.E. Malmström ◽  
B. Meister
Keyword(s):  
Neuropeptide Y ◽  
Rat Kidney ◽  
Y1 Receptor ◽  
Receptor Mrna ◽  
Y1 Receptors

scholarly journals Involvement of Neuropeptide Y Y1 Receptors in the Regulation of Neuroendocrine Corticotropin-Releasing Hormone Neuronal Activity

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3666-3673 ◽  
Author(s):  
Eugene L. Dimitrov ◽  
M. Regina DeJoseph ◽  
Mark S. Brownfield ◽  
Janice H. Urban
Keyword(s):  
Neuropeptide Y ◽  
Hpa Axis ◽  
Binding Protein ◽  
Plasma Corticosterone ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Y1 Receptor ◽  
Element Binding Protein ◽  
Y1 Receptors

The neuroendocrine parvocellular 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 indicated that NPY stimulates CRH mRNA levels. The purpose of these studies was to examine the participation of NPY receptors in HPA axis activation and determine whether neuroendocrine CRH neurons express NPY receptor immunoreactivity. Infusion of 0.5 nmol NPY into the third ventricle increased plasma corticosterone levels in conscious rats, with the peak of hormone levels occurring 30 min after injection. This increase was prevented by pretreatment with the Y1 receptor antagonist BIBP3226. Immunohistochemistry showed that CRH-immunoreactive neurons coexpressed Y1 receptor immunoreactivity (Y1r-ir) in the PVN, and a majority of these neurons (88.8%) were neuroendocrine as determined by ip injections of FluoroGold. Bilateral infusion of the Y1/Y5 agonist, [leu31pro34]NPY (110 pmol), into the PVN increased c-Fos and phosphorylated cAMP response element-binding protein expression and elevated plasma corticosterone levels. Increased expression of c-Fos and phosphorylated cAMP response element-binding protein 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.

Chronic Administration of Glucocorticoids Directly Upregulates Prepro-Neuropeptide Y and Y1-Receptor mRNA Levels in the Arcuate Nucleus of the Rat

1994 ◽  
Vol 6 (2) ◽  
pp. 153-159 ◽  
Author(s):  
Philip J. Larsen ◽  
David S. Jessop ◽  
Hardial S. Chowdrey ◽  
Stafford L. Lightman ◽  
Jens D. Mikkelsen
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Chronic Administration ◽  
Mrna Levels ◽  
Y1 Receptor ◽  
Receptor Mrna

scholarly journals Role of G-protein βγ subunits in the augmentation of P2Y2 (P2U) receptor-stimulated responses by neuropeptide Y Y1 Gi/o-coupled receptors

1997 ◽  
Vol 328 (1) ◽  
pp. 153-158 ◽  
Author(s):  
A. Lisa SELBIE ◽  
V. Natalie KING ◽  
M. John DICKENSON ◽  
J. Stephen HILL
Keyword(s):  
Neuropeptide Y ◽  
G Protein ◽  
Binding Proteins ◽  
Synergistic Interaction ◽  
Y1 Receptor ◽  
Gtp Binding ◽  
Adenosine A1 ◽  
Y1 Receptors ◽  
Stimulation Of

Neuropeptide Y (NPY) significantly potentiates the constrictor actions of noradrenaline and ATP on blood vessels via a pertussis toxin (PTX)-sensitive mechanism involving Gi/o (αβγ) protein subunits (Gi/o, GTP-binding proteins sensitive to PTX). In Chinese hamster ovary K1 (CHO K1) cells expressing specific receptors for these neurotransmitters, stimulation of Gi/o protein-coupled receptors for NPY and other neurotransmitters can augment the Gq/11-coupled (Gq/11, GTP-binding proteins insensitive to PTX) α1B adrenoceptor- or ATP receptor-induced arachidonic acid (AA) release and inositol phosphate (IP) production (early events which may precede vasoconstriction). In this study, we have assessed the role of Gβγ subunits in the synergistic interaction between Gi/o- (NPY Y1, 5-hydroxytryptamine 5-HT1B, adenosine A1) and Gq/11- [ATP P2Y2 (P2U)]-coupled receptors on AA release by using the specific abilities of regions of the β-adrenergic receptor kinase (βARK1 residues 495-689) and the transducin α subunit to associate with G-protein βγ subunit dimers and to act as Gβγ subunit scavengers. Transient expression of βARK1(495-689) in CHO K1 cells heterologously expressing NPY Y1 receptors had no significant effect on the PTX-insensitive ability of ATP to stimulate AA release. Stimulation of NPY Y1 receptors (as well as the endogenous 5-hydroxytryptamine 5-HT1B receptor and the transiently expressed human adenosine A1 receptor) resulted in a PTX-sensitive augmentation of ATP-stimulated AA release, which was inhibited by expression of both Gβγ subunit scavengers. Expression of βARK1(495-689) similarly inhibited NPY Y1 receptor augmentation of ATP-stimulated IP production (a measure of phospholipase C activity), a step thought to precede the NPY Y1 receptor-augmented protein kinase C-dependent AA release previously observed in these cells. These experiments demonstrate that Gβγ subunits, as inhibited by two different Gβγ scavengers, significantly contribute to the synergistic interaction between NPY Y1 Gi/o- and Gq/11-coupled receptor activity, and are required for the augmentation of IP production and AA release observed in this model cell system.

Stress-induced mesenteric vasoconstriction in rats is mediated by neuropeptide Y Y1 receptors

1996 ◽  
Vol 270 (2) ◽  
pp. H796-H800 ◽  
Author(s):  
Z. Zukowska-Grojec ◽  
E. K. Dayao ◽  
E. Karwatowska-Prokopczuk ◽  
G. J. Hauser ◽  
H. N. Doods
Keyword(s):  
Neuropeptide Y ◽  
Vascular Resistance ◽  
Cold Water ◽  
Pressor Response ◽  
Physiological Role ◽  
Y1 Receptor ◽  
Y1 Receptors ◽  
Mesenteric Artery Blood Flow ◽  
Mesenteric Vascular Resistance

The physiological role of neuropeptide Y (NPY), a sympathetic cotransmitter and vasoconstrictor, has not been determined yet. We used a specific nonpeptide antagonist to the NPY Y1 receptor [BIBP-3226; (R)-N2-(diphenacetyl)-N-[(4-hydroxyphenyl) methyl]-D-arginineamide] to study the involvement of NPY in stress-induced vasoconstriction in the mesenteric bed. In rats subjected to cold water stress (COLD), plasma NPY immunoreactivity levels increased progressively from 0.15 +/- 0.01 to 0.32 +/- 0.05 pmol/ml and remained elevated during recovery. Administration of BIBP-3226 (3 mg.kg-1.h-1 infusion) tended to decrease the stress-induced pressor response and significantly attenuated the post-COLD elevation of blood pressure. The COLD-induced fall in the superior mesenteric artery blood flow and the increase of up to 300% in the mesenteric vascular resistance were either reduced or eliminated by BIBP-3226. Conversely, the Y1 antagonist had no effect on the COLD-induced tachycardia. This study provides the first evidence of the physiological role of NPY. The peptide is released during stress and increases mesenteric vascular resistance via activation of its Y1 receptors. Specific Y1-receptor antagonists may therefore be of potential benefit in prevention or treatment of stress-induced vasospasm.

Neuropeptide Y Y1 receptor mRNA in rodent brain: Distribution and colocalization with melanocortin-4 receptor

2004 ◽  
Vol 482 (3) ◽  
pp. 217-243 ◽  
Author(s):  
Toshiro Kishi ◽  
Carl J. Aschkenasi ◽  
Brian J. Choi ◽  
Marisol E. Lopez ◽  
Charlotte E. Lee ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Brain Distribution ◽  
Y1 Receptor ◽  
Receptor Mrna ◽  
Rodent Brain ◽  
Melanocortin 4 Receptor

Localization of neuropeptide Y Y1 receptor mRNA in human tooth pulp

1998 ◽  
Vol 43 (5) ◽  
pp. 389-394 ◽  
Author(s):  
Rolf Uddman ◽  
Joji Kato ◽  
Leonor Cantera ◽  
Lars Edvinsson
Keyword(s):  
Neuropeptide Y ◽  
Human Tooth ◽  
Tooth Pulp ◽  
Y1 Receptor ◽  
Receptor Mrna

scholarly journals Neuropeptide Y Reduces Social Fear in Male Mice: Involvement of Y1 and Y2 Receptors in the Dorsolateral Septum and Central Amygdala

2021 ◽  
Vol 22 (18) ◽  
pp. 10142
Author(s):  
Johannes Kornhuber ◽  
Iulia Zoicas
Keyword(s):  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Receptor Subtypes ◽  
Male Mice ◽  
Central Amygdala ◽  
Contextual Fear ◽  
Y1 Receptor ◽  
Social Fear ◽  
Y1 Receptors ◽  
Prior Administration

Neuropeptide Y (NPY) has anxiolytic-like effects and facilitates the extinction of cued and contextual fear in rodents. We previously showed that intracerebroventricular administration of NPY reduces the expression of social fear in a mouse model of social fear conditioning (SFC) and localized these effects to the dorsolateral septum (DLS) and central amygdala (CeA). In the present study, we aimed to identify the receptor subtypes that mediate these local effects of NPY. We show that NPY (0.1 nmol/0.2 µL/side) reduced the expression of SFC-induced social fear in a brain region- and receptor-specific manner in male mice. In the DLS, NPY reduced the expression of social fear by acting on Y2 receptors but not on Y1 receptors. As such, prior administration of the Y2 receptor antagonist BIIE0246 (0.2 nmol/0.2 μL/side) but not the Y1 receptor antagonist BIBO3304 trifluoroacetate (0.2 nmol/0.2 μL/side) blocked the effects of NPY in the DLS. In the CeA, however, BIBO3304 trifluoroacetate but not BIIE0246 blocked the effects of NPY, suggesting that NPY reduced the expression of social fear by acting on Y1 receptors but not Y2 receptors within the CeA. This study suggests that at least two distinct receptor subtypes are differentially recruited in the DLS and CeA to mediate the effects of NPY on the expression of social fear.

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