Auricular acupuncture decreases neuropeptide Y expression in the hypothalamus of food-deprived Sprague–Dawley rats

2001 ◽  
Vol 307 (2) ◽  
pp. 113-116 ◽  
Author(s):  
Ee-Hwa Kim ◽  
Younhee Kim ◽  
Mi-Hyun Jang ◽  
Baek-Vin Lim ◽  
Youn-Jung Kim ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Auricular Acupuncture ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Postnatal intracerebroventricular exposure to neuropeptide Y causes weight loss in female adult rats

2003 ◽  
Vol 284 (6) ◽  
pp. R1560-R1566 ◽  
Author(s):  
Amit Varma ◽  
Jing He ◽  
Lisa Weissfeld ◽  
Sherin U. Devaskar
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Body Weight Gain ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Sprague Dawley Rats ◽  
Old Adult ◽  
Arcuate Nuclei

We investigated the effect of repetitive postnatal (2–7 days) intracerebroventricular administration of neuropeptide Y (NPY) on food intake and body weight gain in the 3- to 120-day-old Sprague-Dawley rats. NPY caused a 32% transient increase in body weight gain with elevated circulating insulin concentrations within 24 h. This early intervention led to the persistence of hyperinsulinemia and relative hyperleptinemia with euglycemia in the 120-day-old female alone. This perturbation was associated with 50% suppression in adult female hypothalamic NPY concentrations and a 50–85% decline in NPY immunoreactivity in the paraventricular and arcuate nuclei. This change was paralleled by a ∼20% decline in food intake and body weight gain at 60 and 120 days. However, when exogenous NPY was stereotaxically reinjected into the paraventricular nucleus of the ∼120-day-old adult females who were pretreated with NPY postnatally, an increase in food intake and body weight gain was noted, attesting to no disruption in the NPY end-organ responsivity. We conclude that postnatal intracerebroventricular NPY has long-lasting effects that predetermine the resultant adult phenotype in a sex-specific manner.

Anxiety responses and neurochemical changes in a kaolin-induced rat model of hydrocephalus

2011 ◽  
Vol 7 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Yong Sup Hwang ◽  
Insop Shim ◽  
Jin Woo Chang
Keyword(s):  
Neuropeptide Y ◽  
Rat Model ◽  
Elevated Plus Maze ◽  
Sprague Dawley ◽  
Injection Group ◽  
Abnormal Gait ◽  
Sprague Dawley Rats ◽  
Plus Maze ◽  
Anxiety Response ◽  
Neurochemical Changes

Object Hydrocephalus is a pathological enlargement of the ventricles of the brain, which can result from various diseases of the central nervous system. Patients with hydrocephalus frequently show motor abnormalities, such as abnormal gait and posture, as well as intellectual and emotional impairment. The present study was designed to investigate anxiety responses in rats with kaolin-induced hydrocephalus. Methods A total of 26 Sprague-Dawley rats were used for this study. Hydrocephalus was induced in 14 Sprague-Dawley rats by injecting 0.1 ml of 20% kaolin solution into the cisterna magna; 12 rats were administered the same volume of saline in the same fashion and served as controls. Seven of the rats that were injected with kaolin and 6 of the rats injected with saline were killed 3 days after injection (Group 1); the remaining rats were killed 4 weeks after injection (Group 2) to evaluate effects related to acute and chronic hydrocephalus. The rats were tested in an elevated plus maze after induction of hydrocephalus by kaolin injection. After the animals were killed, brain sections were immunostained for cholecystokinin and neuropeptide Y. In addition, tyrosine hydroxlyase immunoreactivity in the ventral tegmental area was evaluated by immunohistological staining. Results The rats with acute hydrocephalus showed decreased entry into and spent less time in the open arms of the elevated plus maze as compared with the control rats. The hydrocephalic rats had significantly more cholecystokinin-immunoreactive neurons and fewer neuropeptide Y–immunoreactive neurons in their brains. In addition, hydrocephalus progress in this model was positively correlated with the anxiety response. The numbers of tyrosine hydroxlyase–immunoreactive neurons were decreased significantly in the hydrocephalic rats as compared with the control rats. Conclusions These results suggest that the rat model of hydrocephalus is characterized by increased anxiety response and is associated with the functional impairment of the central dopamine system.

scholarly journals Neuropeptide Y bioavailability is suppressed in the hindlimb of female Sprague-Dawley rats

2005 ◽  
Vol 568 (2) ◽  
pp. 573-581 ◽  
Author(s):  
Dwayne N. Jackson ◽  
Kevin J. Milne ◽  
Earl G. Noble ◽  
J. Kevin Shoemaker
Keyword(s):  
Neuropeptide Y ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Gender-modulated endogenous baseline neuropeptide Y Y1-receptor activation in the hindlimb of Sprague-Dawley rats

2004 ◽  
Vol 562 (1) ◽  
pp. 285-294 ◽  
Author(s):  
Dwayne N. Jackson ◽  
Kevin J. Milne ◽  
Earl G. Noble ◽  
J. Kevin Shoemaker
Keyword(s):  
Neuropeptide Y ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Y1 Receptor ◽  
Sprague Dawley Rats

scholarly journals Maternal and Postnatal Overnutrition Differentially Impact Appetite Regulators and Fuel Metabolism

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5348-5356 ◽  
Author(s):  
Hui Chen ◽  
David Simar ◽  
Karen Lambert ◽  
Jacques Mercier ◽  
Margaret J. Morris
Keyword(s):  
Neuropeptide Y ◽  
Glucose Transporter ◽  
Maternal Obesity ◽  
Glucose Transporter 4 ◽  
Sprague Dawley ◽  
Metabolic Markers ◽  
Sprague Dawley Rats ◽  
D 20 ◽  
Maternal Overnutrition

Maternal obesity is increasing, and it is known that the intrauterine experience programs fetal and newborn metabolism. However, the relative contributions of pre- or postnatal factors are unknown. We hypothesized that maternal overnutrition caused by long-term maternal obesity would exert a stronger detrimental impact than postnatal overnutrition on offspring metabolic homeostasis, with additional postnatal overnutrition exaggerating these alterations. Female Sprague Dawley rats were exposed to chow or high-fat cafeteria diet for 5 wk before mating and throughout gestation and lactation. On postnatal d 1, litters were adjusted to three per litter to induce postnatal overnutrition (vs. 12 in control). Hypothalamic appetite regulators neuropeptide Y and proopiomelanocortin, glucose transporter 4, and lipid metabolic markers were measured. At postnatal d 20, male pups born of obese dams, or those overnourished postnatally, were 42% heavier than controls; combining both interventions led to 80% greater body weight. Maternal obesity increased pup adiposity and led to glucose intolerance in offspring; these were exaggerated by additional postnatal overnutrition during lactation. Maternal obesity was also linked to hyperlipidemia in offspring and reduced hypothalamic neuropeptide Y and increased proopiomelanocortin mRNA expression. Postnatal overnutrition of offspring from obese dams amplified these hypothalamic changes. Both maternal and postnatal overnutrition reduced muscle glucose transporter 4. Adipose carnitine palmitoyl-transferase-1 and adipose triglyceride lipase mRNA was up-regulated only by postnatal overnutrition. Maternal overnutrition appears to alter central appetite circuits and promotes early-onset obesity; postnatal overnutrition interacted to cause peripheral lipid and glucose metabolic disorders, supporting the critical message to reduce early-life adverse nutritional impact.

Agonist-Induced Release of Neuropeptide Y by Platelets

1996 ◽  
Vol 9 (1) ◽  
pp. 1-8
Author(s):  
A. Torres Duarte ◽  
Z. Zukowska-Grojec ◽  
A.K. Myers
Keyword(s):  
Platelet Aggregation ◽  
Immune Responses ◽  
Neuropeptide Y ◽  
Platelet Rich Plasma ◽  
High Dose ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Irreversible Aggregation ◽  
Dose Dependent

Neuropeptide Y (NPY) is a multi-functional peptide localized in a number of tissues besides the brain, and its expression is high in strains of mice with autoimmune disease. Functionally, along with its neurotransmitter role, NPY has multiple effects on both vascular tissues and tissues involved in immune responses. Previous studies demonstrated that immunoreactive NPY (i-NPY) exists in large quantities in platelets and bone marrow of some species, and suggested its release during platelet aggregation by collagen. Because NPY has been hypothesized to have a role in a number of pathophysiological states in which platelets are involved, including immune responses, hypertension and vascular smooth muscle proliferation, we sought to further characterize platelet i-NPY content and release by a diverse group of physiological platelet agonists. Platelet rich plasma and gel filtered platelets were prepared from citrated whole blood of male Sprague Dawley rats. Platelet content and concentration of i-NPY were quantified by RIA. Platelet aggregation responses (turbidometric method) and release of i-NPY were measured in rat platelet preparations stimulated by a thromboxane agonist (U44069), collagen, thrombin and ADP. All agents induced dose-dependent aggregation, although ADP and U44069 were weak agonists in citrated platelet rich plasma, ADP only inducing primary aggregation. Total i-NPY content in platelet rich plasma of Sprague-Dawley rats was 32.1±3.8 pmol/ml; more than 20 pmol/ml was released into supernatant of aggregating platelets stimulated with high dose thrombin or collagen during secondary, irreversible aggregation. Although U44069 and ADP both stimulated i-NPY release in a dose-dependent manner, release was substantially lower than with the other agonists. We conclude that i-NPY release from rat platelets is associated mainly with secondary, irreversible aggregation, and can be produced by a variety of platelet stimulating agents as part of the platelet release reaction. The present study and other recent studies demonstrate wide variability in platelet i-NPY content between and within species. Investigation of the genetic regulation of i-NPY content in platelets could offer new insights into the relationship between NPY and pathophysiology of the immune and cardiovascular systems.

Endogenous neuropeptide Y regulates thyroid blood flow

1993 ◽  
Vol 264 (5) ◽  
pp. E699-E705 ◽  
Author(s):  
M. Michalkiewicz ◽  
L. J. Huffman ◽  
M. Dey ◽  
G. A. Hedge
Keyword(s):  
Neuropeptide Y ◽  
Thyroid Stimulating Hormone ◽  
Nerve Fibers ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Sympathetic Nerve Fibers ◽  
Arterial Blood ◽  
Sprague Dawley Rats

Neuropeptide Y (NPY) is present in thyroid sympathetic nerve fibers. To assess the involvement of endogenous NPY in the regulation of thyroid function, a NPY antiserum was produced in a rabbit, characterized, and used for immunization of normal and hyperthyroid rats. Plasma thyroxine, thyroid-stimulating hormone (TSH), thyroidal, and other organ blood flows (BF) were measured in anesthetized (ketamine and pentobarbital sodium) male Sprague-Dawley rats at 1 h after intravenous administration of 1 ml of the antiserum, normal rabbit serum, or saline. Immunization against NPY had no effect on the plasma levels of thyroxine, TSH, or arterial blood pressure, but it significantly increased thyroidal BF in normal rats. In the hyperthyroid rats (treated with 5 micrograms.100 g body wt-.day-1 thyroxine for 6 days), the NPY antiserum reversed the hyperthyroidism-induced decrease in thyroid BF and significantly increased duodenal and testicular BF values, but it did not alter BF values in four other organs. These results indicate that endogenous NPY regulates thyroid BF in normal rats. They also provide an example of NPY involvement in the pathophysiological adjustment of some organs to hyperthyroidism.

Sign in / Sign up

Export Citation Format

Share Document