Localization of neuropeptide Y-immunoreactive cells and fibres in the brain of the Japanese quail

1991 ◽  
Vol 265 (2) ◽  
pp. 219-230 ◽  
Author(s):  
N. Aste ◽  
C. Viglietti-Panzica ◽  
A. Fasolo ◽  
C. Andreone ◽  
H. Vaudry ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Japanese Quail ◽  
The Brain

scholarly journals The Role of Neuropeptide Y in the Nucleus Accumbens

2021 ◽  
Vol 22 (14) ◽  
pp. 7287
Author(s):  
Masaki Tanaka ◽  
Shunji Yamada ◽  
Yoshihisa Watanabe
Keyword(s):  
Nervous System ◽  
Nucleus Accumbens ◽  
Neuropeptide Y ◽  
Emotional Behavior ◽  
Characteristic Functions ◽  
Receptor Subtypes ◽  
Neuroendocrine Mechanisms ◽  
Fear And Anxiety ◽  
The Brain

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.

Multifaces of neuropeptide Y in the brain – Neuroprotection, neurogenesis and neuroinflammation

Neuropeptides ◽  
2012 ◽  
Vol 46 (6) ◽  
pp. 299-308 ◽  
Author(s):  
J.O. Malva ◽  
S. Xapelli ◽  
S. Baptista ◽  
J. Valero ◽  
F. Agasse ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
The Brain

Neuropeptide Y Receptors: Autoradiographic Distribution in the Brain and Structure-Activity Relationships

1990 ◽  
Vol 611 (1 Central and P) ◽  
pp. 58-72 ◽  
Author(s):  
RÉMI QUIRION ◽  
JEAN-CLAUDE MARTEL ◽  
YVAN DUMONT ◽  
ALAIN CADIEUX ◽  
FRANCOIS JOLICOEUR ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Structure Activity Relationships ◽  
Structure Activity ◽  
The Brain ◽  
Y Receptors ◽  
Neuropeptide Y Receptors

Dexamethasone rapidly increases hypothalamic neuropeptide Y secretion in adrenalectomized ob/ob mice

1996 ◽  
Vol 271 (1) ◽  
pp. E151-E158 ◽  
Author(s):  
H. L. Chen ◽  
D. R. Romsos
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Rapid Onset ◽  
Brown Adipose ◽  
Specific Enhancement ◽  
Brown Adipose Tissue Thermogenesis ◽  
The Central Nervous System ◽  
Rapid Transport ◽  
The Brain

A single intracerebroventricular injection of dexamethasone (DEX) rapidly (within 30 min) suppresses brown adipose tissue thermogenesis and increases plasma insulin concentrations in adrenal-ectomized (ADX) ob/ob mice but not in ADX lean mice. Intracerebroventricular neuropeptide Y (NPY) administered intracerebroventricularly causes these same metabolic changes within 30 min in both ob/ob and lean ADX mice. We therefore hypothesized that DEX exerts these rapid-onset metabolic actions in ob/ob mice via a phenotype-specific enhancement of NPY secretion within the central nervous system. In support of this hypothesis, DEX (a type II glucocorticoid receptor agonist) administered intracerebroventricularly selectively lowered NPY concentrations in the whole hypothalamus of ADX ob/ob mice by 35% and in the arcuate nucleus region by approximately 70% within 30 min but not in the brain stem or hippocampus or in any of these regions of lean mice. DEX also functioned in vitro to enhance depolarization-dependent release of NPY from hypothalamic blocks of ADX ob/ob mice but not of ADX lean mice. Thus DEX acts in the hypothalamus of ob/ob mice in a phenotype-specific manner to evoke rapid transport of NPY from cell bodies within the arcuate nucleus to terminal regions including the dorsomedial and ventromedial hypothalamic regions for release.

Interaction between neuropeptide Y immunoreactive neurons and galanin immunoreactive neurons in the brain of the masu salmon, Oncorhynchus masou

2009 ◽  
Vol 462 (1) ◽  
pp. 33-38 ◽  
Author(s):  
Masafumi Amano ◽  
Noriko Amiya ◽  
Mikiko Hiramatsu ◽  
Takuma Tomioka ◽  
Yoshitaka Oka
Keyword(s):  
Neuropeptide Y ◽  
Masu Salmon ◽  
Oncorhynchus Masou ◽  
The Brain ◽  
Masu Salmon Oncorhynchus Masou

Characterization of the Brain Penetrant Neuropeptide Y Y2 Receptor Antagonist SF-11

2019 ◽  
Vol 10 (8) ◽  
pp. 3454-3463 ◽  
Author(s):  
Helena Domin ◽  
Natalia Piergies ◽  
Ewa Pięta ◽  
Elżbieta Wyska ◽  
Bartłomiej Pochwat ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Y2 Receptor ◽  
The Brain

scholarly journals Neuropeptide Y in normal eating and in genetic and dietary-induced obesity

2006 ◽  
Vol 361 (1471) ◽  
pp. 1159-1185 ◽  
Author(s):  
B Beck
Keyword(s):  
Neuropeptide Y ◽  
Diet Composition ◽  
High Energy ◽  
Glucose Sensing ◽  
Feeding Regulation ◽  
Treatment Of Obesity ◽  
The Brain ◽  
Diet Type

Neuropeptide Y (NPY) is one the most potent orexigenic peptides found in the brain. It stimulates food intake with a preferential effect on carbohydrate intake. It decreases latency to eat, increases motivation to eat and delays satiety by augmenting meal size. The effects on feeding are mediated through at least two receptors, the Y1 and Y5 receptors. The NPY system for feeding regulation is mostly located in the hypothalamus. It is formed of the arcuate nucleus (ARC), where the peptide is synthesized, and the paraventricular (PVN), dorsomedial (DMN) and ventromedial (VMN) nuclei and perifornical area where it is active. This activity is modulated by the hindbrain and limbic structures. It is dependent on energy availability, e.g. upregulation with food deprivation or restriction, and return to baseline with refeeding. It is also sensitive to diet composition with variable effects of carbohydrates and fats. Leptin signalling and glucose sensing which are directly linked to diet type are the most important factors involved in its regulation. Absence of leptin signalling in obesity models due to gene mutation either at the receptor level, as in the Zucker rat, the Koletsky rat or the db / db mouse, or at the peptide level, as in ob / ob mouse, is associated with increased mRNA abundance, peptide content and/or release in the ARC or PVN. Other genetic obesity models, such as the Otsuka–Long–Evans–Tokushima Fatty rat, the agouti mouse or the tubby mouse, are characterized by a diminution in NPY expression in the ARC nucleus and by a significant increase in the DMN. Further studies are necessary to determine the exact role of NPY in these latter models. Long-term exposure to high-fat or high-energy palatable diets leads to the development of adiposity and is associated with a decrease in hypothalamic NPY content or expression, consistent with the existence of a counter-regulatory mechanism to diminish energy intake and limit obesity development. On the other hand, an overactive NPY system (increased mRNA expression in the ARC associated with an upregulation of the receptors) is characteristic of rats or rodent strains sensitive to dietary-induced obesity. Finally, NPY appears to play an important role in body weight and feeding regulation, and while it does not constitute the only target for drug treatment of obesity, it may nevertheless provide a useful target in conjunction with others.

Sign in / Sign up

Export Citation Format

Share Document