Bombesin, but not amylin, blocks the orexigenic effect of peripheral ghrelin

2006 ◽  
Vol 291 (4) ◽  
pp. R903-R913 ◽  
Author(s):  
Peter Kobelt ◽  
Miriam Goebel ◽  
Andreas Stengel ◽  
Marco Schmidtmann ◽  
Ivo R. van der Voort ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuronal Activity ◽  
Paraventricular Nucleus ◽  
Arcuate Nucleus ◽  
Vehicle Group ◽  
Fos Expression ◽  
Crf Neurons ◽  
Stimulation Of

The interaction between ghrelin and bombesin or amylin administered intraperitoneally on food intake and brain neuronal activity was assessed by Fos-like immunoreactivity (FLI) in nonfasted rats. Ghrelin (13 μg/kg ip) increased food intake compared with the vehicle group when measured at 30 min (g/kg: 3.66 ± 0.80 vs. 1.68 ± 0.42, P < 0.0087). Bombesin (8 μg/kg) injected intraperitoneally with ghrelin (13 μg/kg) blocked the orexigenic effect of ghrelin (1.18 ± 0.41 g/kg, P < 0.0002). Bombesin alone (4 and 8 μg/kg ip) exerted a dose-related nonsignificant reduction of food intake (g/kg: 1.08 ± 0.44, P > 0.45 and 0.55 ± 0.34, P > 0.16, respectively). By contrast, ghrelin-induced stimulation of food intake (g/kg: 3.96 ± 0.56 g/kg vs. vehicle 0.82 ± 0.59, P < 0.004) was not altered by amylin (1 and 5 μg/kg ip) (g/kg: 4.37 ± 1.12, P > 0.69, and 3.01 ± 0.78, respectively, P > 0.37). Ghrelin increased the number of FLI-positive neurons/section in the arcuate nucleus (ARC) compared with vehicle (median: 42 vs. 19, P < 0.008). Bombesin alone (4 and 8 μg/kg ip) did not induce FLI neurons in the paraventricular nucleus of the hypothalamus (PVN) and coadministered with ghrelin did not alter ghrelin-induced FLI in the ARC. However, bombesin (8 μg/kg) with ghrelin significantly increased neuronal activity in the PVN approximately threefold compared with vehicle and ∼1.5-fold compared with the ghrelin group. Bombesin (8 μg/kg) with ghrelin injected intraperitoneally induced Fos expression in 22.4 ± 0.8% of CRF-immunoreactive neurons in the PVN. These results suggest that peripheral bombesin, unlike amylin, inhibits peripheral ghrelin induced food intake and enhances activation of CRF neurons in the PVN.

CCK inhibits the orexigenic effect of peripheral ghrelin

2005 ◽  
Vol 288 (3) ◽  
pp. R751-R758 ◽  
Author(s):  
Peter Kobelt ◽  
Johannes J. Tebbe ◽  
Ines Tjandra ◽  
Andreas Stengel ◽  
Hi-Gung Bae ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuronal Activity ◽  
Arcuate Nucleus ◽  
Ingestive Behavior ◽  
Vehicle Group ◽  
Reduce Food Intake ◽  
Nonsignificant Trend ◽  
Fos Expression ◽  
Stimulation Of ◽  
Cumulative Food Intake

CCK and ghrelin exert antagonistic effects on ingestive behavior. The aim of the present study was to investigate the interaction between ghrelin and CCK administered peripherally on food intake and neuronal activity in specific hypothalamic and brain stem nuclei, as assessed by c-Fos-like immunoreactivity (c-FLI) in nonfasted rats. Ghrelin (13 μg/kg body wt) injected intraperitoneally significantly increased the cumulative food intake when measured at 30 min and 1 h after injection, compared with the vehicle group (2.9 ± 1.0 g/kg body wt vs. 1.2 ± 0.5 g/kg body wt, P < 0.028). Sulfated CCK octapeptide (CCK-8S) (2 or 25 μg/kg body wt) injected simultaneously blocked the orexigenic effect of ghrelin (0.22 ± 0.13 g/kg body wt, P < 0.001 and 0.33 ± 0.23 g/kg body wt, P < 0.0008), while injected alone, both doses of CCK-8S exerted a nonsignificant trend to reduce food intake. Ghrelin (13 μg/kg body wt ip) markedly increased the number of c-FLI-positive neurons per section in the arcuate nucleus (ARC) compared with vehicle (median: 31.35 vs. 9.86, P < 0.0001). CCK-8S (2 or 25 μg/kg body wt ip) had no effect on neuronal activity in the ARC, as assessed by c-FLI (median: 5.33 and 11.21 cells per section), but blocked the ghrelin-induced increase of c- fos expression in this area when both peptides were administered simultaneously (median: 13.33 and 12.86 cells per section, respectively). Ghrelin at this dose had no effect on CCK-induced stimulation of c- fos expression in the paraventricular nucleus of the hypothalamus and the nucleus of the solitary tract. These results suggest that CCK abolishes ghrelin-induced food intake through dampening increased ARC neuronal activity.

Apolipoprotein A-IV interacts synergistically with melanocortins to reduce food intake

2006 ◽  
Vol 290 (1) ◽  
pp. R202-R207 ◽  
Author(s):  
Koro Gotoh ◽  
Min Liu ◽  
Stephen C. Benoit ◽  
Deborah J. Clegg ◽  
W. Sean Davidson ◽  
...  
Keyword(s):  
Food Intake ◽  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Arcuate Nucleus ◽  
Reduce Food Intake ◽  
The Third ◽  
Apolipoprotein A ◽  
Anorectic Effect ◽  
Fos Expression ◽  
Long Evans

Apolipoprotein (apo) A-IV is an anorexigenic gastrointestinal peptide that is also synthesized in the hypothalamus. The goal of these experiments was to determine whether apo A-IV interacts with the central melanocortin (MC) system in the control of feeding. The third ventricular (i3vt) administration of a subthreshold dose of apo A-IV (0.5 μg) potentiated i3vt MC-induced (metallothionein-II, 0.03 nmol) suppression of 30-min feeding in Long-Evans rats. A subthreshold dose of the MC antagonist (SHU9119, 0.1 nmol, i3vt) completely attenuated the anorectic effect of i3vt apo A-IV (1.5 μg). The i3vt apo A-IV significantly elevated the expression of c-Fos in neurons of the paraventricular nucleus of the hypothalamus, but not in the arcuate nucleus or median eminence. In addition, c-Fos expression was not colocalized with proopiomelanocortin-positive neurons. These data support a synergistic interaction between apo A-IV and melanocortins that reduces food intake by acting downstream of the arcuate.

scholarly journals GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

2015 ◽  
Vol 309 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Paraventricular Nucleus ◽  
Wistar Rats ◽  
Arcuate Nucleus ◽  
Chemical Stimulation ◽  
Nucleus Ambiguus ◽  
Glycine Receptors ◽  
Inhibitory Neurotransmitters ◽  
Hypothalamic Arcuate Nucleus ◽  
Male Wistar Rats ◽  
Stimulation Of

We have previously reported that stimulation of the hypothalamic arcuate nucleus (ARCN) by microinjections of N-methyl-d-aspartic acid (NMDA) elicits tachycardia, which is partially mediated via inhibition of vagal inputs to the heart. The neuronal pools and neurotransmitters in them mediating tachycardia elicited from the ARCN have not been identified. We tested the hypothesis that the tachycardia elicited from the ARCN may be mediated by inhibitory neurotransmitters in the nucleus ambiguus (nAmb). Experiments were done in urethane-anesthetized, artificially ventilated, male Wistar rats. In separate groups of rats, unilateral and bilateral microinjections of muscimol (1 mM), gabazine (0.01 mM), and strychnine (0.5 mM) into the nAmb significantly attenuated tachycardia elicited by unilateral microinjections of NMDA (10 mM) into the ARCN. Histological examination of the brains showed that the microinjections sites were within the targeted nuclei. Retrograde anatomic tracing from the nAmb revealed direct bilateral projections from the ARCN and hypothalamic paraventricular nucleus to the nAmb. The results of the present study suggest that tachycardia elicited by stimulation of the ARCN by microinjections of NMDA is mediated via GABAA and glycine receptors located in the nAmb.

Factors from paraventricular nucleus mediating adrenocorticotropin release in cats

1987 ◽  
Vol 252 (1) ◽  
pp. R109-R121
Author(s):  
D. E. Carlson ◽  
D. S. Gann
Keyword(s):  
Paraventricular Nucleus ◽  
Corticotropin Releasing Factor ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Immunocytochemical Localization ◽  
Before And After ◽  
Alpha Chloralose ◽  
Crf Neurons ◽  
Caudal Area ◽  
Stimulation Of

Experiments were conducted in alpha-chloralose-urethan-anesthetized cats. We stimulated the hypothalamic paraventricular nucleus (PVH) electrically before and after intracerebroventricular (icv) injection of an antiserum to arginine vasopressin (AVP), one to corticotropin-releasing factor (CRF), or one to normal rabbit serum (NRS). Stimulation of the ventral portion of the dorsal PVH led to increases in arterial pressure and heart rate that did not change after any of the icv treatments. However, the effect of each agent on the increases in plasma adrenocorticotropin (ACTH) after stimulation was related to the area of the PVH that was stimulated. The response to stimulation of a rostral area that extended dorsally from the anterior PVH was blocked completely by the anti-AVP but not by anti-CRF or NRS. The response to stimulation of a caudal area located in the dorsal PVH was attenuated after anti-CRF, unchanged after anti-AVP, and augmented after NRS. The antibodies that were given icv were found immunocytochemically to enter the median eminence at sites that include some adjacent to the portal vessels. Immunocytochemical localization of AVP- and of CRF-containing neurons in the PVH showed that the anterior PVH had the highest proportion of AVP neurons in the PVH but had only a few CRF neurons. In contrast, the dorsal PVH contained the highest density of CRF neurons in the PVH as well as some AVP neurons. We suggest that, in the cat, the primary releasing factor for the anterior PVH is AVP and that for the dorsal PVH is CRF.

Stimulation of food intake after central galanin is associated with arcuate nucleus activation and does not differ between genetically selected low and high body weight lines of chickens

Neuropeptides ◽  
2013 ◽  
Vol 47 (4) ◽  
pp. 281-285 ◽  
Author(s):  
Christopher J. Hagen ◽  
Brandon A. Newmyer ◽  
Rebekah I. Webster ◽  
Elizabeth R. Gilbert ◽  
Paul B. Siegel ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Arcuate Nucleus ◽  
High Body Weight ◽  
High Body ◽  
Stimulation Of

scholarly journals Neuropeptide S Stimulates the Hypothalamo-Pituitary-Adrenal Axis and Inhibits Food Intake

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3510-3518 ◽  
Author(s):  
Kirsty L. Smith ◽  
Michael Patterson ◽  
Waljit S. Dhillo ◽  
Sejal R. Patel ◽  
Nina M. Semjonous ◽  
...  
Keyword(s):  
Food Intake ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Arginine Vasopressin ◽  
Lateral Ventricle ◽  
Neuropeptide S ◽  
Plasma Acth ◽  
Vasopressin Release ◽  
Pituitary Adrenal Axis ◽  
Stimulation Of

Neuropeptide S (NPS) is a recently discovered peptide shown to be involved in the modulation of arousal and fear responses. It has also been shown that lateral ventricle administration of NPS causes a significant decrease in food intake. Neuropeptides involved in the modulation of arousal have been shown to be involved in the regulation of the hypothalamo-pituitary adrenal (HPA) axis and food intake. In this study, we have examined the effect of intracerebroventricular (ICV) administration of NPS on behavior, regulation of the HPA axis, and food intake. ICV NPS significantly increased plasma ACTH and corticosterone 10 and 40 min after injection, respectively. A single ICV injection of NPS caused a significant increase in rearing activity as well as ambulatory movement for up to 45 min after injection. We then studied the effect of paraventricular nucleus (PVN) administration of NPS on the regulation of the HPA axis, behavior, and food intake. There was a significant increase in plasma ACTH and corticosterone after a single NPS PVN injection. Incubation of hypothalamic explants with increasing concentrations of NPS caused a significant increase in CRH and arginine vasopressin release. In addition, PVN administration of NPS dose-dependently inhibited food intake in the first hour after injection, although no effect on food intake was seen after this time. PVN administration of NPS caused a significant increase in rearing activity. These data demonstrate a novel role for NPS in the stimulation of the HPA axis.

Effect of galanin on food intake in rats: involvement of lateral and ventromedial hypothalamic sites

1993 ◽  
Vol 264 (2) ◽  
pp. R355-R361 ◽  
Author(s):  
R. R. Schick ◽  
S. Samsami ◽  
J. P. Zimmermann ◽  
T. Eberl ◽  
C. Endres ◽  
...  
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Paraventricular Nucleus ◽  
Lateral Hypothalamus ◽  
Ventromedial Hypothalamus ◽  
Initial Increase ◽  
Intracerebroventricular Injection ◽  
Fasted Rats ◽  
Stimulation Of ◽  
Cumulative Food Intake

Galanin has previously been reported to elicit feeding in satiated animals when injected into the hypothalamic paraventricular nucleus. It is not known, however, 1) whether this action is due to activation of feeding signals or suppression of satiety signals or both or 2) whether other hypothalamic regions such as the lateral hypothalamus (LH) or the ventromedial hypothalamus (VMH) are involved in this action. The effects of galanin on food intake were therefore examined in satiated and in fasted rats both after intracerebroventricular injection (0.1, 1, and 10 micrograms/10 microliters) and after microinjection (1 and 5 micrograms/0.5 microliters) into the LH and VMH. Twenty minutes after intracerebroventricular injection, galanin significantly and dose dependently augmented food intake by up to sevenfold in freely feeding rats and by up to 79% in fasted animals. The galanin-induced augmentation of cumulative food intake up to 2 h after injection was due to the initial increase in food consumption during the 0 to 20-min interval. This suggests that galanin acts by activation of feeding behavior and not by suppression of satiety signals in these fasted animals, in which satiety signals are presumably not initially operative. Twenty minutes after intrahypothalamic injections into both the LH and VMH, galanin (5 micrograms) significantly increased food consumption, fivefold in freely feeding rats and 30-35% in fasted rats. Thus stimulation of feeding by centrally injected galanin also involves loci within the LH and VMH.

Neurochemical phenotype of hypothalamic neurons showing Fos expression 23 h after intracranial AgRP

2002 ◽  
Vol 282 (6) ◽  
pp. R1773-R1781 ◽  
Author(s):  
Huiyuan Zheng ◽  
Michele M. Corkern ◽  
Scott M. Crousillac ◽  
Laurel M. Patterson ◽  
Curtis B. Phifer ◽  
...  
Keyword(s):  
Food Intake ◽  
Lateral Hypothalamus ◽  
Arcuate Nucleus ◽  
Light Phase ◽  
Melanocortin 4 Receptor ◽  
Significant Difference ◽  
Melanin Concentrating Hormone ◽  
Double Label ◽  
Fos Expression ◽  
Agouti Related Protein

Agouti-related protein (AgRP) is coexpressed with neuropeptide Y (NPY) in a population of neurons in the arcuate nucleus (ARC) of the hypothalamus and stimulates food intake for up to 7 days if injected intracerebroventricularly. The prolonged food intake stimulation does not seem to depend on continued competition at the melanocortin-4 receptor (MC4R), because the relatively specific MC4R agonist MTII regains its ability to suppress food intake 24 h after AgRP injection. Intracerebroventricular AgRP also stimulates c-Fos expression 24 h after injection in several brain areas, so the neurons exhibiting delayed Fos expression might be particularly important in feeding behavior. Thus we aimed to identify the neurochemical phenotype of some of these neurons in select hypothalamic areas, using double-label immunohistochemistry. AgRP-injected rats ingested significantly more chow (10.2 ± 0.6 g) vs. saline controls (3.4 ± 0.7 g) in the first 9 h (light phase) after injection. In the lateral hypothalamus (particularly the perifornical area) 23 h after injection, AgRP induced significantly more Fos vs. saline in orexin-A (OXA) neurons (25.6 ± 4.9 vs. 4.8 ± 3.1%), but not in melanin-concentrating hormone (MCH) or cocaine- and amphetamine-regulated transcript (CART) neurons. In the ARC, AgRP induced significantly more Fos in CART (40.6 ± 5.9 vs. 13.4 ± 1.8%) but not NPY neurons. In the paraventricular nucleus, there was no significant difference in Fos expression induced by AgRP vs. saline in oxytocin and CART neurons. We conclude that the long-lasting hyperphagia induced by AgRP is correlated with and possibly partially mediated by hyperactive OXA neurons in the lateral hypothalamus and CART neurons in the ARC, but not by NPY and MCH neurons. The substantial increase in light-phase food intake by AgRP supports a role for the arousing effects of OXA. Activation of CART neurons in the ARC (which likely coexpress proopiomelanocortin) could indicate attempts to activate counterregulatory decreases in food intake.

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