Caudal hindbrain participation in the suppression of feeding by central and peripheral bombesin

1993 ◽  
Vol 264 (6) ◽  
pp. R1229-R1234 ◽  
Author(s):  
E. E. Ladenheim ◽  
R. C. Ritter
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Cerebral Ventricle ◽  
Solitary Tract ◽  
Medial Nucleus ◽  
Neural Substrate

We have previously demonstrated that bombesin (BBS) infused into the fourth cerebral ventricle in rats suppressed feeding at doses 10-1,000 times less than those required after lateral ventricular administration. These results suggest that centrally administered BBS acts in the caudal hindbrain to suppress food intake. To investigate the participation of caudal hindbrain structures in fourth-ventricular BBS-induced suppression of feeding, we made lesions that destroyed the following: 1) area postrema (AP) and 2) and medial nucleus of the solitary tract (NST). Additionally, we examined the role of the AP/NST in the suppression of food intake after peripheral BBS administration. Our experiments revealed that lesions of the AP/NST abolished the suppression of food intake by fourth-ventricular BBS and attenuated the suppression of food intake by peripheral BBS. Lesions restricted to the AP attenuated the suppression of food intake by fourth-ventricular BBS but had no effect on suppression of intake by peripherally administered BBS. These results suggest that the NST may be a common neural substrate for the inhibition of food intake by both centrally and peripherally administered BBS.

Role of area postrema in control of torpor in Siberian hamsters

2000 ◽  
Vol 279 (2) ◽  
pp. R591-R598 ◽  
Author(s):  
Helen H. Bae ◽  
Juliet L. Stamper ◽  
Eric C. Heydorn ◽  
Irving Zucker ◽  
John Dark
Keyword(s):  
Food Intake ◽  
Food Restriction ◽  
Area Postrema ◽  
Solitary Tract ◽  
Metabolic Fuel ◽  
Short Day ◽  
Siberian Hamsters ◽  
Metabolic Challenge ◽  
Short Days

Siberian hamsters undergo torpor during the short days of winter and in response to glucoprivation or food restriction. We tested whether the area postrema and the adjacent nucleus of the solitary tract (hereafter the AP), which monitor metabolic fuel availability, also control the onset of torpor. Siberian hamsters that had manifested torpor spontaneously or had entered torpor in response to 2-deoxy-d-glucose (2-DG) treatment were subjected to area postrema ablations (APx). Hamsters continued to display torpor postoperatively; most features of torpor were unaffected by APx. The AP is not necessary for expression of torpor elicited by short day lengths or metabolic challenge. In contrast, decreases in food intake manifested by hamsters treated with 2-DG were counteracted by APx. In Siberian hamsters, the AP appears to mediate effects of 2-DG on food intake but not torpor.

Central leptin modulates behavioral and neural responsivity to CCK

1999 ◽  
Vol 276 (5) ◽  
pp. R1545-R1549 ◽  
Author(s):  
Michael Emond ◽  
Gary J. Schwartz ◽  
Ellen E. Ladenheim ◽  
Timothy H. Moran
Keyword(s):  
Food Intake ◽  
Paraventricular Nucleus ◽  
Area Postrema ◽  
Protein Product ◽  
Liquid Diet ◽  
Solitary Tract ◽  
Ob Gene ◽  
Medial Nucleus

The mechanisms through which leptin, the protein product of the ob gene, affects food intake remain to be determined. To assess whether the actions of leptin depend on modulation of within-meal satiety signals, we measured the effect of third ventricular leptin administration on the satiety actions of CCK. Leptin (10 μg) administered 1 h before 30-min access to a liquid diet had no effect on intake when administered alone, but doses of 3.5 or 10 μg dose dependently increased the suppression of intake produced by 1 nmol/kg CCK. Examination of patterns of c-Fos activation induced by 3.5 μg leptin and 1 nmol/kg CCK revealed that the combination produced significant c-Fos activation within the area postrema and the caudal and medial nucleus of the solitary tract (NST) compared with either leptin or CCK treatments alone. The leptin-CCK combination also resulted in increased c-Fos activation within the paraventricular nucleus of the hypothalamus above that produced by leptin alone. These data suggest that the actions of leptin in food intake are mediated through its ability to modulate responsivity to within-meal satiety signals.

Noradrenergic neurons of the area postrema mediate amylin's hypophagic action

2010 ◽  
Vol 299 (2) ◽  
pp. R623-R631 ◽  
Author(s):  
Catarina S. Potes ◽  
Victoria F. Turek ◽  
Rebecca L. Cole ◽  
Calvin Vu ◽  
Barbara L. Roland ◽  
...  
Keyword(s):  
Food Intake ◽  
Low Dose ◽  
Area Postrema ◽  
Solitary Tract ◽  
Noradrenergic Neurons ◽  
Neuronal Activation ◽  
Fos Protein ◽  
Noradrenaline Synthesis ◽  
Fos Expression

Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim of this study was to identify the neurochemical phenotype of the neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression of c-Fos protein was used as a marker for neuronal activation and dopamine-β-hydroxylase (DBH), the enzyme-catalyzing noradrenaline synthesis, as a marker for noradrenergic neurons. We found that ∼50% of amylin-activated AP neurons are noradrenergic. To clarify the functional role of these neurons in amylin's effect on eating, noradrenaline-containing neurons in the AP were lesioned using a saporin conjugated to an antibody against DBH. Amylin (5 or 20 μg/kg sc)-induced anorexia was observed in sham-lesioned rats with both amylin doses. Rats with a lesion of > 50% of the noradrenaline neurons were unresponsive to the low dose of amylin (5 μg/kg) and only displayed a reduction in food intake 60 min after injection of the high amylin dose (20 μg/kg). In a terminal experiment, the same rats received amylin (20 μg/kg) or saline. The AP and nucleus of the solitary tract (NTS) were stained for DBH to assess noradrenaline lesion success and for c-Fos expression to evaluate amylin-induced neuronal activation. In contrast to sham-lesioned animals, noradrenaline-lesioned rats did not show a significant increase in amylin-induced c-Fos expression in the AP and NTS. We conclude that the noradrenergic neurons in the AP mediate at least part of amylin's hypophagic effect.

Area postrema and adjacent nucleus of the solitary tract in water and sodium balance

1984 ◽  
Vol 247 (1) ◽  
pp. R173-R182 ◽  
Author(s):  
T. M. Hyde ◽  
R. R. Miselis
Keyword(s):  
Water Deprivation ◽  
Area Postrema ◽  
Sodium Balance ◽  
Solitary Tract ◽  
Nacl Solution ◽  
Medial Nucleus

Lesions of the area postrema (AP) and adjacent caudal medial nucleus of the solitary tract (cmNTS) cause significant changes in water and sodium balance. Lesioned rats display a permanent polydipsia, which in part is due to a primary polyuria. Water-to-food ratios are elevated chronically. Lesioned rats are unable to concentrate their urine as well as controls. In addition, lesioned rats overdrink in response to 24-h water deprivation. This lesion also causes a natriuresis and an overconsumption of 3% NaCl solution. These findings establish the AP-cmNTS as an important part of the neurocircuitry underlying water and sodium balance.

Lateral parabrachial lesions attenuate ingestive effects of area postrema lesions

1989 ◽  
Vol 256 (2) ◽  
pp. R306-R312 ◽  
Author(s):  
G. L. Edwards ◽  
R. C. Ritter
Keyword(s):  
Short Duration ◽  
Area Postrema ◽  
Parabrachial Nucleus ◽  
Solitary Tract ◽  
Palatable Food ◽  
Lateral Parabrachial Nucleus ◽  
Ingestive Behaviors

Lesions of the area postrema and adjacent nucleus of the solitary tract (AP lesions) cause rats to consume increased amounts of palatable food in short duration tests. Because the lateral parabrachial nucleus (lPBN) receives a prominent afferent projection from the AP and adjacent nucleus of the solitary tract, it is possible the lPBN plays a role in the altered ingestive behaviors observed in AP-lesioned rats. The present study examines the role of the lPBN in overingestion of highly palatable foods subsequent to AP lesions. We found that lesions of the lPBN alone did not cause rats to consume increased amounts of palatable food. Rather, when lPBN lesions were produced before AP lesions, increased intake of highly palatable food did not occur. Moreover, when AP-lesioned rats received subsequent lPBN lesions, the previously established overingestion of palatable foods was abolished. These results indicate that the lPBN is necessary in the pathogenesis of AP lesion-induced overingestion of highly palatable foods.

Body weight of rats following area postrema ablation: effect of early force-feeding

1989 ◽  
Vol 256 (4) ◽  
pp. R939-R945
Author(s):  
N. J. Kenney ◽  
J. N. Kott ◽  
N. Tomoyasu ◽  
A. J. Bhatia ◽  
A. S. Ruiz ◽  
...  
Keyword(s):  
Body Weight ◽  
Preliminary Analysis ◽  
Area Postrema ◽  
Solitary Tract ◽  
Milk Diet ◽  
Medial Nucleus ◽  
Body Weights ◽  
Force Feeding ◽  
Ad Libitum ◽  
Ad Libitum Feeding

This study examined the effect of intragastric force-feeding of a milk diet on body weights of rats with lesions of the area postrema/caudal medial nucleus of the solitary tract (AP/cmNTS). Force-feeding was conducted over the first 10 days after the ablation. Body weight was monitored both during and after force-feeding. Food intake was measured during all ad libitum feeding periods. During force-feeding, rats with AP/cmNTS lesions gained weight at the same rate as force-fed sham-lesioned rats or sham-lesioned rats that voluntarily ingested an equal amount of the milk. When returned to ad libitum feeding, lesioned rats that had been force-fed were not hypophagic and did not lose weight. Body weights of such rats remained above those of lesioned rats that were not force-fed and similar to those of nonlesioned rats throughout this study. Despite their normal weights, preliminary analysis indicated that body fat of the force-fed lesioned rats may have been reduced. These findings suggest that the effects of AP/cmNTS ablation are multiple and that reduction of body weight need not be the primary effect of such lesions.

Area postrema mediates tumor effects on food intake, body weight, and learned aversions

1985 ◽  
Vol 249 (3) ◽  
pp. R296-R300 ◽  
Author(s):  
I. L. Bernstein ◽  
C. M. Treneer ◽  
J. N. Kott
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Leydig Cell ◽  
Area Postrema ◽  
Solitary Tract ◽  
Medial Area

Growth of a Leydig cell [LTW (m)] tumor in rats is associated with the development of significant hypophagia and severe aversions to the available diet. Lesions of the area postrema and nearby caudal medial area of the solitary tract were found to block or greatly attenuate the anorexia and food aversions that typically accompany the growth of this tumor. Thus these tumor-induced symptoms may be associated with the detection of blood-borne chemicals by cells located in or near the area postrema.

scholarly journals Endogenous leptin receptor signaling in the medial nucleus tractus solitarius affects meal size and potentiates intestinal satiation signals

2012 ◽  
Vol 303 (4) ◽  
pp. E496-E503 ◽  
Author(s):  
Scott E. Kanoski ◽  
Shiru Zhao ◽  
Douglas J. Guarnieri ◽  
Ralph J. DiLeone ◽  
Jianqun Yan ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Leptin Receptor ◽  
Nucleus Tractus Solitarius ◽  
Balance Control ◽  
Area Postrema ◽  
Meal Size ◽  
Receptor Signaling ◽  
Medial Nucleus ◽  
Neuronal Systems

Leptin receptor (LepRb) signaling in the hindbrain is required for energy balance control. Yet the specific hindbrain neurons and the behavioral processes mediating energy balance control by hindbrain leptin signaling are unknown. Studies here employ genetic [adeno-associated virally mediated RNA interference (AAV-RNAi)] and pharmacological methodologies to specify the neurons and the mechanisms through which hindbrain LepRb signaling contributes to the control of food intake. Results show that AAV-RNAi-mediated LepRb knockdown targeting a region encompassing the mNTS and area postrema (AP) (mNTS/AP LepRbKD) increases overall cumulative food intake by increasing the size of spontaneous meals. Other results show that pharmacological hindbrain leptin delivery and RNAi-mediated mNTS/AP LepRb knockdown increased and decreased the intake-suppressive effects of intraduodenal nutrient infusion, respectively. These meal size and intestinally derived signal amplification effects are likely mediated by LepRb signaling in the mNTS and not the AP, since 4th icv and mNTS parenchymal leptin (0.5 μg) administration reduced food intake, whereas this dose did not influence food intake when injected into the AP. Overall, these findings deepen the understanding of the distributed neuronal systems and behavioral mechanisms that mediate the effects of leptin receptor signaling on the control of food intake.

Neural substrate for an integrated metabolic control of feeding behavior

1999 ◽  
Vol 276 (1) ◽  
pp. R113-R119 ◽  
Author(s):  
Charles C. Horn ◽  
Aleymayehu Addis ◽  
Mark I. Friedman
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Metabolic Control ◽  
Area Postrema ◽  
Integrated Control ◽  
Combined Treatment ◽  
Brain Regions ◽  
Metabolic Inhibitors ◽  
Acid Oxidation ◽  
Neural Substrate

Evidence indicates that feeding behavior in rats is controlled by a mechanism that integrates information about different aspects of fuel metabolism. We investigated the neural substrate for this integrated control by measuring the effect of metabolic inhibitors given alone and in combination on food intake and neuronal activity as reflected by the expression of c-Fos protein. Combined administration of methyl palmoxirate (5 mg/kg po), an inhibitor of fatty acid oxidation, and 2,5-anhydro-d-mannitol (150 mg/kg ip), which decreases liver ATP content, increased feeding in rats more than expected on the basis of eating responses after treatment with either inhibitor given alone. Combined treatment also produced a synergistic increase in Fos-like immunoreactivity in several brain areas, including the nucleus of the solitary tract, area postrema, and parvocellular portion of the hypothalamic paraventricular nucleus. These findings provide strong evidence for the involvement of selected brain regions in the metabolic control of food intake and suggest that metabolic information used to control feeding behavior is integrated in the periphery or at the level of the brain stem.

Glucoprivic treatments that induce anestrus, but do not affect food intake, increase FOS-like immunoreactivity in the area postrema and nucleus of the solitary tract in Syrian hamsters

1995 ◽  
Vol 698 (1-2) ◽  
pp. 107-113 ◽  
Author(s):  
Jill E. Schneider ◽  
Bridget C. Finnerty ◽  
Jennifer M. Swann ◽  
Jean Marie Gabriel
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Solitary Tract ◽  
Syrian Hamsters
Sign in / Sign up

Export Citation Format

Share Document