Urocortin 1 administered into the hypothalamic supraoptic nucleus inhibits food intake in freely fed and food-deprived rats

Amino Acids ◽  
2012 ◽  
Vol 44 (3) ◽  
pp. 879-885 ◽  
Author(s):  
A. Fatima ◽  
S. Andrabi ◽  
G. Wolf ◽  
M. Engelmann ◽  
M. G. Spina
Keyword(s):  
Food Intake ◽  
Supraoptic Nucleus ◽  
Urocortin 1 ◽  
Hypothalamic Supraoptic Nucleus

Urocortin 1 administered into the hypothalamic supraoptic nucleus affects open-field behaviour in rats

Amino Acids ◽  
2009 ◽  
Vol 38 (5) ◽  
pp. 1407-1414 ◽  
Author(s):  
Ambrin Fatima ◽  
M. Fahad Haroon ◽  
Gerald Wolf ◽  
Mario Engelmann ◽  
Mariarosa G. Spina
Keyword(s):  
Open Field ◽  
Supraoptic Nucleus ◽  
Urocortin 1 ◽  
Field Behaviour ◽  
Hypothalamic Supraoptic Nucleus ◽  
Open Field Behaviour

LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Inhibitory Action ◽  
Functional Implications ◽  
Urocortin 1 ◽  
Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

EFFECTS OF CHEMORECEPTOR AND BARORECEPTOR STIMULATION ON THE DISCHARGE OF HYPOTHALAMIC SUPRAOPTIC NEURONES IN RATS

1979 ◽  
Vol 82 (1) ◽  
pp. 115-125 ◽  
Author(s):  
M. C. HARRIS
Keyword(s):  
Supraoptic Nucleus ◽  
Carotid Sinus ◽  
Carotid Bifurcation ◽  
Cardiovascular Reflexes ◽  
Nacl Solution ◽  
Baroreceptor Stimulation ◽  
Vasopressin Secretion ◽  
Carotid Body Chemoreceptors ◽  
Hypothalamic Supraoptic Nucleus ◽  
Slight Inhibition

SUMMARY Experiments have been performed to examine the effects of activating the carotid body chemoreceptors and the arterial baroreceptors on the discharge of neurones within the hypothalamic supraoptic nucleus of the rat. Chemoreceptors were activated by intracarotid injection of 0·9% NaCl solution equilibrated with 100% CO2. The baroreceptors of the carotid sinus and aortic arch were activated by raising the blood pressure with an intravenous injection of phenylephrine. Chemoreceptor stimulation activated and baroreceptor stimulation inhibited the discharge of all the phasically discharging neurones tested. Neither stimulus had any consistent effect on non-phasically discharging neurones, although slight inhibition occasionally occurred. Anaesthesia of the carotid bifurcation abolished the effects of cardiovascular stimulation on the supraoptic neurones. Responses resumed when the anaesthesia wore off. However, the anaesthesia also seemed to alter the phasic pattern of discharge. The results are discussed with reference to the influence of the cardiovascular receptors upon the neurones in the supraoptic nucleus, and with reference to possible roles for the cardiovascular reflexes in control of vasopressin secretion.

Oxytocin in the periaqueductal gray mainly comes form the hypothalamic supraoptic nucleus to participate in pain modulation

Peptides ◽  
2019 ◽  
Vol 121 ◽  
pp. 170153
Author(s):  
Wen-Quan Jiang ◽  
Le-Le Bao ◽  
Fang-Jie Sun ◽  
Xi-Lin Liu ◽  
Jun Yang
Keyword(s):  
Supraoptic Nucleus ◽  
Periaqueductal Gray ◽  
Pain Modulation ◽  
Hypothalamic Supraoptic Nucleus

Hypothalamic mapping of orexigenic action and Fos-like immunoreactivity following relaxin-3 administration in male Wistar rats

2007 ◽  
Vol 292 (3) ◽  
pp. E913-E919 ◽  
Author(s):  
B. M. McGowan ◽  
S. A. Stanley ◽  
N. E. White ◽  
A. Spangeus ◽  
M. Patterson ◽  
...  
Keyword(s):  
Food Intake ◽  
Supraoptic Nucleus ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Disulphide Bonds ◽  
Hypothalamic Nuclei ◽  
Relaxin Family ◽  
Male Wistar Rats ◽  
Additional Support ◽  
G Protein Coupled

The insulin superfamily, characterized by common disulphide bonds, includes not only insulin but also insulin-like peptides such as relaxin-1 and relaxin-3. The actions of relaxin-3 are largely unknown, but recent work suggests a role in regulation of food intake. Relaxin-3 mRNA is highly expressed in the nucleus incertus, which has extensive projections to the hypothalamus, and relaxin immunoreactivity is present in several hypothalamic nuclei. In the rat, relaxin-3 binds and activates both relaxin family peptide receptor 1, which also binds relaxin-1, and a previously orphaned G protein-coupled receptor, RXFP3. These receptors are extensively expressed in the hypothalamus. The aims of these studies were twofold: 1) map the hypothalamic site(s) of the orexigenic action of relaxin-3 and 2) examine the site(s) of neuronal activation following central relaxin-3 administration. After microinjection into hypothalamic sites, human relaxin-3 (H3; 180 pmol) significantly stimulated 0- to 1-h food intake in the supraoptic nucleus (SON), arcuate nucleus (ARC), and the anterior preoptic area (APOA) [SON 0.4 ± 0.2 (vehicle) vs. 2.9 ± 0.5 g (H3), P < 0.001; ARC 0.7 ± 0.3 (vehicle) vs. 2.7 ± 0.2 g (H3), P < 0.05; and APOA 0.8 ± 0.1 (vehicle) vs. 2.2 ± 0.2 g (H3), P < 0.05]. Cumulative food intake was significantly increased ≤8 h following administration into the SON and 4 h into the APOA. A significant increase in Fos-like immunoreactivity was seen in the SON following central relaxin-3 administration. Relaxin-3 stimulates feeding in several hypothalamic nuclei, and these studies provide additional support for relaxin-3 as an important peptide in appetite regulation.

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