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.

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.

Sodium appetite and Fos activation in serotonergic neurons

2002 ◽  
Vol 282 (1) ◽  
pp. R235-R243 ◽  
Author(s):  
Lucia F. Franchini ◽  
Alan Kim Johnson ◽  
José de Olmos ◽  
Laura Vivas
Keyword(s):  
Peritoneal Dialysis ◽  
Area Postrema ◽  
Sodium Balance ◽  
Not Given ◽  
Nacl Solution ◽  
Sodium Depletion ◽  
Serotonergic Neurons ◽  
Sodium Appetite ◽  
Sodium Ingestion ◽  
Solution Intake

We evaluated serotonergic hindbrain groups of cells for their involvement in the generation and inhibition of sodium appetite. For that purpose, we analyzed the number of Fos-immunoreactive (Fos-ir) cells and double-labeled Fos-serotonin (5-HT)-ir neurons within different nuclei of the hindbrain raphe system and the area postrema (AP). Sodium depletion and sodium appetite were induced by peritoneal dialysis. Twenty-four hours after peritoneal dialysis, a 2% NaCl solution intake test was given to peritoneal dialyzed animals [PD-with access (PD-A) group] and to control dialyzed animals [CD-with access (CD-A) group]. Two additional groups of animals received either peritoneal dialysis or control dialysis but were not given access to the 2% NaCl [CD-no access (CD-NA) group or PD-no access (PD-NA) group]. The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. The PD-NA group had significantly fewer double-labeled cells along the raphe system compared with the animals in near-normal sodium balance (CD-NA and CD-A) or in the process of restoring sodium balance by consuming NaCl (PD-A). The AP of the PD-A group showed a significant increase in the number of Fos-ir and Fos-5-HT-ir cells compared with the PD-NA and CD groups. Our results suggest that serotonergic pathways with cell bodies in the AP and the raphe system are involved in the control of sodium appetite.

Impaired osmoregulatory responses in rats with area postrema lesions

1999 ◽  
Vol 277 (1) ◽  
pp. R209-R219 ◽  
Author(s):  
Kathleen S. Curtis ◽  
Wan Huang ◽  
Alan F. Sved ◽  
Joseph G. Verbalis ◽  
Edward M. Stricker
Keyword(s):  
Adult Male ◽  
Sodium Excretion ◽  
Area Postrema ◽  
Hormone Secretion ◽  
Male Rats ◽  
Salt Appetite ◽  
Solitary Tract ◽  
Nacl Solution ◽  
Water Ingestion ◽  
Nacl Load

Area postrema lesions (APX) in adult male rats produced a robust spontaneous intake of 0.5 M NaCl, as reported previously. The largest NaCl intakes (up to 108 ml/day) were observed when there was little incidental damage in the medial subnucleus of the nucleus of the solitary tract adjacent to the caudal and middle portions of the area postrema. Rats with discrete APX also drank substantial amounts of 0.5 M NaCl when access to saline was restricted to 7 h/day (up to 30 ml in 1 h, 48 ml in 7 h). Such large NaCl intakes stimulated considerable water ingestion and renal sodium excretion, but together these responses usually were insufficient for osmoregulation during the 7-h test period. After systemic administration of hypertonic NaCl solution, rats with APX excreted less Na+ in urine and secreted less vasopressin and oxytocin than control rats did. The prominent salt appetite, insufficient thirst and natriuresis in response to an ingested NaCl load, and blunted natriuresis and neurohypophysial hormone secretion in response to an injected NaCl load, all indicate that osmoregulatory responses are impaired in rats after APX.

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.

Effects of area postrema/caudal medial nucleus of solitary tract lesions on food intake and body weight

1983 ◽  
Vol 244 (4) ◽  
pp. R577-R587 ◽  
Author(s):  
T. M. Hyde ◽  
R. R. Miselis
Keyword(s):  
Body Weight ◽  
Area Postrema ◽  
Body Weight Loss ◽  
Solitary Tract ◽  
Medial Nucleus ◽  
Nucleus Of Solitary Tract ◽  
Lower Body Weight ◽  
High Fat Diets ◽  
Fat Diets ◽  
Dorsal Medulla

Lesions of the area postrema/caudal medial nucleus of the solitary tract (AP/cmNTS), located on the surface of the dorsal medulla of the rat, cause a transient syndrome of hypophagia and body weight loss, with the establishment of a new growth curve at a lower body weight set point. The regulatory responses to prolonged food deprivation, glucoprivic stimulation, and chronic access to a palatable diet are left largely intact. However, there is an overconsumption of highly palatable foods during acute exposure to supermarket and high-fat diets. Intestinal transit and gastric retention are unaffected by the lesion, indicating normal motor function within the gastrointestinal system. The hypophagia and chronic depression of body weight by the AP/cmNTS lesion demonstrate that this area is an important part of the larger neurocircuitry subserving feeding behavior and energy balance.

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.

Water deprivation-induced sodium appetite and differential expression of encephalic c-Fos immunoreactivity in the spontaneously hypertensive rat

2010 ◽  
Vol 298 (5) ◽  
pp. R1298-R1309 ◽  
Author(s):  
Daniela T. B. Pereira-Derderian ◽  
Regina C. Vendramini ◽  
José V. Menani ◽  
Laurival A. De Luca
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Spontaneously Hypertensive Rat ◽  
Area Postrema ◽  
Cell Activity ◽  
Sodium Balance ◽  
Lamina Terminalis ◽  
Spontaneously Hypertensive ◽  
Sodium Appetite ◽  
Hypertensive Rat

The spontaneously hypertensive rat (SHR) has an intense consumption of NaCl solution. Water deprivation (WD) followed by water intake to satiety induces partial rehydration (PR)—the WD-PR protocol—and sodium appetite. In the present work, WD produced similar water intake and no alterations in arterial pressure among spontaneously hypertensive rat (SHR), Wistar-Kyoto, and Holtzman strains. It also increased the number of cells with positive c-Fos immunoreactivity (Fos-IR) in the lamina terminalis and in the hypothalamic supraoptic (SON) and paraventricular (parvocellular, PVNp) nucleus in these strains. The WD and WD-PR produced similar alterations in all strains in serum osmolality and protein, plasma renin activity, and sodium balance. The SHR ingested about 10 times more 0.3 M NaCl than normotensives strains in the sodium appetite test that follows WD-PR. After WD-PR, the Fos-IR persisted, elevated in the lamina terminalis of all strains but notably in the subfornical organ of the SHR. The WD-PR reversed Fos-IR in the SON of all strains and in the PVNp of SHR. It induced Fos-IR in the area postrema and in the nucleus of the solitary tract (NTS), dorsal raphe, parabrachial (PBN), pre-locus coeruleus (pre-LC), suprachiasmatic, and central amygdalar nucleus of all strains. This effect was bigger in the caudal-NTS, pre-LC, and medial-PBN of SHRs. The results indicate that WD-PR increases cell activity in the forebrain and hindbrain areas that control sodium appetite in the rat. They also suggest that increased cell activity in facilitatory brain areas precedes the intense 0.3 M NaCl intake of the SHR in the sodium appetite test.

Rat brainstem neurons responsive to changes in portal blood sodium concentration

1984 ◽  
Vol 247 (5) ◽  
pp. R792-R799 ◽  
Author(s):  
P. J. Kahrilas ◽  
R. C. Rogers
Keyword(s):  
Hypertonic Saline ◽  
Choline Chloride ◽  
Vena Cava ◽  
Sodium Concentration ◽  
Portal Blood ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Response Characteristics ◽  
Medial Nucleus ◽  
Rat Brainstem

Studies were performed to identify the response characteristics of nucleus of the solitary tract neurons receiving afferent projections from the hepatic branch of the vagus nerve. Thirty Sprague-Dawley rats under pentobarbital anesthesia had catheters placed in the ileocolic vein and the inferior vena cava. Neuronal recordings were made in the left medial nucleus of the solitary tract (NST), in the area where hepatic vagal fibers terminate. Sixteen NST cells were identified that responded selectively to the portal infusion of water or hypertonic saline. Two patterns of response were seen: 1) 12 neurons were persistently stimulated by portal hypertonic saline and persistently inhibited by portal water, and 2) four neurons were either transiently excited (n = 3) or transiently inhibited (n = 1) by portal hypertonic saline with no water effect. All units recorded responded to changes of 1% or less in portal blood sodium concentration. Hypertonic mannitol was an ineffective stimulus but choline chloride was as effective as sodium chloride. This suggests that the hepatic receptors utilize an Na+-K+-ATPase electrogenic pump in the transduction process.

scholarly journals Centrally and Peripherally Administered Ghrelin Potently Inhibits Water Intake in Rats

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1638-1647 ◽  
Author(s):  
Hirofumi Hashimoto ◽  
Hiroaki Fujihara ◽  
Makoto Kawasaki ◽  
Takeshi Saito ◽  
Minori Shibata ◽  
...  
Keyword(s):  
Food Intake ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Intravenous Injection ◽  
Water Intake ◽  
Water Deprivation ◽  
Area Postrema ◽  
Urine Volume ◽  
The Brain ◽  
Atrial Natriuretic

Ghrelin is known as a potent orexigenic hormone through its action on the brain. In this study, we examined the effects of intracerebroventricular (icv) and iv injection of ghrelin on water intake, food intake, and urine volume in rats deprived of water for 24 h. Water intake that occurred after water deprivation was significantly inhibited by icv injection of ghrelin (0.1, 1, and 10 nmol/rat) in a dose-related manner, although food intake was stimulated by the hormone. The antidipsogenic effect was as potent as the orexigenic effect. Similarly, water intake was inhibited, whereas food intake was stimulated dose dependently after iv injection of ghrelin (0.1, 1, and 10 nmol/kg). The inhibition of drinking was comparable with, or even more potent than, atrial natriuretic peptide (ANP), an established antidipsogenic hormone, when administered icv, although the antidipsogenic effect lasted longer. ANP had no effect on food intake. Urine volume decreased dose relatedly after icv injection of ghrelin but not by ANP. Intravenous injection of ghrelin had no effect on urine volume. Because drinking usually occurs with feeding, food was withdrawn to remove the prandial drinking. Then the antidipsogenic effect of ghrelin became more potent than that of ANP and continued longer than when food was available. Expression of Fos was increased in the area postrema and the nucleus of the tractus solitarius by using immunohistochemistry after icv and iv injection of ghrelin. The present study convincingly showed that ghrelin is a potent antidisogenic peptide in rats.

GABAergic Pump Cells of Solitary Tract Nucleus Innervate Retrotrapezoid Nucleus Chemoreceptors

2007 ◽  
Vol 98 (1) ◽  
pp. 374-381 ◽  
Author(s):  
Ana C. Takakura ◽  
Thiago S. Moreira ◽  
Gavin H. West ◽  
Justin M. Gwilt ◽  
Eduardo Colombari ◽  
...  
Keyword(s):  
Area Postrema ◽  
Inhibitory Neurons ◽  
Acid Decarboxylase ◽  
Solitary Tract ◽  
Vagus Nerves ◽  
Toxin B ◽  
Lung Inflation ◽  
Retrotrapezoid Nucleus ◽  
Nucleus Of Solitary Tract ◽  
Tracheal Pressure

The retrotrapezoid nucleus (RTN) contains central respiratory chemoreceptors that are inhibited by activation of slowly adapting pulmonary stretch receptors (SARs). Here we examine whether RTN inhibition by lung inflation could be mediated by a direct projection from SAR second-order neurons (pump cells). Pump cells ( n = 56 neurons, 13 rats) were recorded in the nucleus of solitary tract (NTS) of halothane-anesthetized rats with intact vagus nerves. Pump cells had discharges that coincided with lung inflation as monitored by the tracheal pressure. Their activity increased when end-expiratory pressure was raised and stopped instantly when ventilation was interrupted in expiration. Many pump cells could be antidromically activated from RTN (12/36). Nine of those were labeled with biotinamide. Of these nine cells, eight contained glutamic acid decarboxylase 67 (GAD67) mRNA and seven were found to reside in the lower half of the interstitial subnucleus of NTS (iNTS). Using the retrograde tracer cholera toxin-B, we confirmed that neurons located in or close to iNTS innervate RTN (two rats). Many such neurons contained GAD67 mRNA and a few contained glycine transporter2 (GLYT2) mRNA. Anterograde tract tracing with biotinylated dextranamide (four rats) applied to iNTS also confirmed that this region innervates RTN by a predominantly GABAergic projection. This work confirms that many rat NTS pump cells are located in and around the interstitial subnucleus at area postrema level. We demonstrate that a GABAergic subset of these pump cells innervates the RTN region. We conclude that these inhibitory neurons probably contact RTN chemoreceptors and mediate their inhibition by lung inflation.

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