The role of the paraventricular nucleus of the thalamus in the augmentation of heroin seeking induced by chronic food restriction

2019 ◽  
Vol 25 (2) ◽  
Author(s):  
Alexandra Chisholm ◽  
Jessica Iannuzzi ◽  
Damaris Rizzo ◽  
Natasha Gonzalez ◽  
Émilie Fortin ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Food Restriction ◽  
Chronic Food Restriction

Role of ghrelin in metabolic and neuroendocrine adaptations to undernutrition in a mouse model of chronic food restriction

2017 ◽  
Vol 27 ◽  
pp. S1121
Author(s):  
E.Y. Berreby ◽  
A. Labarthe ◽  
P. Zizzari ◽  
P. Durriez ◽  
M. Mequinion ◽  
...  
Keyword(s):  
Mouse Model ◽  
Food Restriction ◽  
Chronic Food Restriction

scholarly journals Is it stress? The role of stress related systems in chronic food restriction-induced augmentation of heroin seeking in the rat

2013 ◽  
Vol 7 ◽  
Author(s):  
Firas Sedki ◽  
Zarish Abbas ◽  
Staci Angelis ◽  
Jeffrey Martin ◽  
Tracey D'Cunha ◽  
...  
Keyword(s):  
Food Restriction ◽  
Chronic Food Restriction

Role of 17-β-estradiol and progesterone on glucose homeostasis: Effects of food restriction (50%) in pregnant and non pregnant rats

1997 ◽  
Vol 20 (7) ◽  
pp. 397-403 ◽  
Author(s):  
C. G. González ◽  
F. D. García ◽  
S. F. Ferníndez ◽  
Angeles M. Patterson
Keyword(s):  
Glucose Homeostasis ◽  
Food Restriction ◽  
Pregnant Rats

scholarly journals The effects of chronic food restriction on cue-induced heroin seeking in abstinent male rats

2012 ◽  
Vol 225 (1) ◽  
pp. 241-250 ◽  
Author(s):  
Tracey M. D’Cunha ◽  
Firas Sedki ◽  
Josie Macri ◽  
Cristina Casola ◽  
Uri Shalev
Keyword(s):  
Food Restriction ◽  
Male Rats ◽  
Chronic Food Restriction

Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats

1994 ◽  
Vol 266 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
S. C. Malpas ◽  
J. H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Neuronal Cell ◽  
Detection Algorithm ◽  
Homocysteic Acid ◽  
Renal Sympathetic Nerve Activity ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Peak Detection Algorithm ◽  
Glass Micropipette

Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were recorded. A computerized sympathetic peak-detection algorithm was applied to recordings of sympathetic discharges to retrieve information about the characteristics of RSNA during PVN stimulation. The algorithm scanned the series of RSNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RSNA peak had been detected, its corresponding amplitude and peak-to-peak interval were calculated. PVN stimulation consistently increased the amplitude of RSNA (mean 30 +/- 5.6% over control), arterial pressure, and the peak-to-peak interval of discharges. A V1 vasopressin antagonist intrathecally administered as a 500-pmol dose was subsequently able to completely block the hemodynamic response (blood pressure increase of 14 +/- 5%) and a 35 +/- 6% increase in RSNA in response to PVN stimulation and intrathecal vasopressin. Thus spinal vasopressin is likely to be a neurotransmitter involved in the cardiovascular regulation involving the PVN.

scholarly journals Temporal changes in nutritional state affect hypothalamic POMC peptide levels independently of leptin in adult male mice

2014 ◽  
Vol 306 (8) ◽  
pp. E904-E915 ◽  
Author(s):  
Aaron J. Mercer ◽  
Ronald C. Stuart ◽  
Courtney A. Attard ◽  
Veronica Otero-Corchon ◽  
Eduardo A. Nillni ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Restriction ◽  
Fluorescent Protein ◽  
Negative Energy ◽  
Nutritional State ◽  
Melanocyte Stimulating Hormone ◽  
Reporter Mice ◽  
State Affect ◽  
Plasma Leptin ◽  
Chronic Food Restriction

Hypothalamic proopiomelanocortin (POMC) neurons constitute a critical anorexigenic node in the central nervous system (CNS) for maintaining energy balance. These neurons directly affect energy expenditure and feeding behavior by releasing bioactive neuropeptides but are also subject to signals directly related to nutritional state such as the adipokine leptin. To further investigate the interaction of diet and leptin on hypothalamic POMC peptide levels, we exposed 8- to 10-wk-old male POMC- Discosoma red fluorescent protein (DsRed) transgenic reporter mice to either 24–48 h (acute) or 2 wk (chronic) food restriction, high-fat diet (HFD), or leptin treatment. Using semiquantitative immunofluorescence and radioimmunoassays, we discovered that acute fasting and chronic food restriction decreased the levels of adrenocorticotropic hormone (ACTH), α-melanocyte-stimulating hormone (α-MSH), and β-endorphin in the hypothalamus, together with decreased DsRed fluorescence, compared with control ad libitum-fed mice. Furthermore, acute but not chronic HFD or leptin administration selectively increased α-MSH levels in POMC fibers and increased DsRed fluorescence in POMC cell bodies. HFD and leptin treatments comparably increased circulating leptin levels at both time points, suggesting that transcription of Pomc and synthesis of POMC peptide products are not modified in direct relation to the concentration of plasma leptin. Our findings indicate that negative energy balance persistently downregulated POMC peptide levels, and this phenomenon may be partially explained by decreased leptin levels, since these changes were blocked in fasted mice treated with leptin. In contrast, sustained elevation of plasma leptin by HFD or hormone supplementation did not significantly alter POMC peptide levels, indicating that enhanced leptin signaling does not chronically increase Pomc transcription and peptide synthesis.

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