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.

Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis

1999 ◽  
Vol 276 (4) ◽  
pp. R1180-R1187 ◽  
Author(s):  
Lucia F. Franchini ◽  
Laura Vivas
Keyword(s):  
Peritoneal Dialysis ◽  
Area Postrema ◽  
Neuronal Population ◽  
Sodium Balance ◽  
Sodium Appetite ◽  
Lateral Parabrachial Nucleus ◽  
Sodium Ingestion ◽  
Oxytocinergic Neurons ◽  
Neuronal Groups ◽  
Sodium Consumption

Fos immunoreactivity was used to map the neuronal population groups activated after sodium ingestion induced by peritoneal dialysis (PD) in rats. Oxytocin immunoreactivity in combination with Fos immunoreactivity was also analyzed to evaluate whether the oxytocinergic neurons of the paraventricular nucleus of the hypothalamus (PVN) are activated during the satiety process of sodium appetite. Sodium ingestion stimulated by PD produced Fos immunoreactivity within defined cells groups of the lamina terminalis and hindbrain areas such us the nucleus of the solitary tract, area postrema, and lateral parabrachial nucleus. On the other hand, particular parvocellular and magnocellular oxytocinergic subdivisions of the PVN and supraoptic nucleus were double labeled after PD-induced sodium consumption. Approximately 27 and 2.1%, respectively, of the activated dorsomedial cap and parvocellular posterior subnuclei of the PVN, which project to the hindbrain, were oxytocinergic. Our data indicate that specific neuronal groups are activated during the satiety process of sodium appetite, suggesting they may form a circuit subserving sodium balance regulation. They also support a functional role for the oxytocinergic neurons in this circuit.

scholarly journals Effect of sex chromosome complement on sodium appetite and Fos-immunoreactivity induced by sodium depletion

2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Area Postrema ◽  
Brain Activity ◽  
Chromosome Complement ◽  
Circumventricular Organs ◽  
Sexually Dimorphic ◽  
Sodium Depletion ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet

Previous studies indicate a sex chromosome complement (SCC) effect on the angiotensin II-sexually dimorphic hypertensive and bradycardic baroreflex responses. We sought to evaluate whether SCC may differentially modulate sexually dimorphic-induced sodium appetite and specific brain activity due to physiological stimulation of the rennin angiotensin system. For this purpose, we used the “four core genotype” mouse model, in which the effect of gonadal sex and SCC is dissociated, allowing comparisons of sexually dimorphic traits between XX and XY females as well as in XX and XY males. Gonadectomized mice were sodium depleted by furosemide (50 mg/kg) and low-sodium diet treatment; control groups were administered with vehicle and maintained on normal sodium diet. Twenty-one hours later, the mice were divided into two groups: one group was submitted to the water-2% NaCl choice intake test, while the other group was perfused and their brains subjected to the Fos-immunoreactivity (FOS-ir) procedure. Sodium depletion, regardless of SCC (XX or XY), induced a significantly lower sodium and water intake in females than in males, confirming the existence in mice of sexual dimorphism in sodium appetite and the organizational involvement of gonadal steroids. Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis.

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.

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.

Rapid-onset "need-free" sodium appetite after lesions of the dorsomedial medulla

1993 ◽  
Vol 264 (6) ◽  
pp. R1242-R1247 ◽  
Author(s):  
G. L. Edwards ◽  
T. G. Beltz ◽  
J. D. Power ◽  
A. K. Johnson
Keyword(s):  
Area Postrema ◽  
Extracellular Fluid ◽  
Rapid Onset ◽  
Sodium Balance ◽  
Bilateral Nephrectomy ◽  
Sodium Appetite ◽  
Fluid Compartment ◽  
Sodium Loss ◽  
Ad Libitum Intake ◽  
Saline Solutions

Previous studies indicate the dorsomedial hindbrain is important in the maintenance of fluid balance. Lesions centering on the area postrema (AP) result in enhanced ad libitum intake of concentrated saline solutions on a 24-h basis as well as enhanced excretion of water and electrolytes. Additionally, rats with lesions of the AP are reported to have an exaggerated behavioral response to dipsogenic challenges that mimic depletion of the extracellular fluid compartment. In the studies reported here, we have observed that rats with lesions of the AP and immediately adjacent nucleus of the solitary tract consume large quantities of concentrated saline solutions within minutes of presentation. This intake does not appear to be related to sodium loss or depletion because the lesioned rats are in a positive sodium balance and the appetite persists after bilateral nephrectomy. These data, in conjunction with earlier studies, suggest that the dorsomedial medulla, including the AP, acts to prevent overconsumption of water and sodium that could result in increased extracellular fluid volume.

scholarly journals Parabrachial and hypothalamic interaction in sodium appetite

2011 ◽  
Vol 300 (5) ◽  
pp. R1091-R1099 ◽  
Author(s):  
S. Dayawansa ◽  
S. Peckins ◽  
S. Ruch ◽  
R. Norgren
Keyword(s):  
Weight Loss ◽  
Lateral Hypothalamus ◽  
Ibotenic Acid ◽  
The Other ◽  
Salt Appetite ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Parabrachial Nuclei ◽  
Bilateral Lesions

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

Effect of Changes in Sodium Balance on Potassium/Aldosterone Dose-Response Curves in the Dog

1982 ◽  
Vol 62 (4) ◽  
pp. 373-380 ◽  
Author(s):  
M. G. Nicholls ◽  
M. Tree ◽  
J. H. Livesey ◽  
R. Fraser ◽  
J. J. Morton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Depletion ◽  
Beagle Dogs ◽  
Response Curves ◽  
Dose Response Curves

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone responses were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose—response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose—response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4–6 mmol/l. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.

Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis

1995 ◽  
Vol 268 (6) ◽  
pp. R1401-R1405 ◽  
Author(s):  
M. el Ghissassi ◽  
S. N. Thornton ◽  
S. Nicolaidis
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
High Sensitivity ◽  
Ang Ii ◽  
Nacl Solution ◽  
At1 Receptors ◽  
Sodium Appetite ◽  
Specific Antagonist

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.

scholarly journals Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

2018 ◽  
Vol 50 (10) ◽  
pp. 904-912 ◽  
Author(s):  
Fatima Trebak ◽  
Wencheng Li ◽  
Yumei Feng
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Total Fluid Intake ◽  
Sodium Deficiency ◽  
Sodium Appetite ◽  
The Central Nervous System ◽  
Salt Sensitive Hypertension

Increased sodium appetite is a physiological response to sodium deficiency; however, it has also been implicated in disease conditions such as congestive heart failure, kidney failure, and salt-sensitive hypertension. The central nervous system is the major regulator of sodium appetite and intake behavior; however, the neural mechanisms underlying this behavior remain incompletely understood. Here, we investigated the involvement of the (pro)renin receptor (PRR), a component of the brain renin-angiotensin system, in the regulation of sodium intake in a neuron-specific PRR knockout (PRRKO) mouse model generated previously in our laboratory. Sodium intake following deoxycorticosterone (DOCA) stimulation was tested by assessing the preference of mice for 0.9% saline or regular water in single-animal metabolic cages. Blood pressure was monitored in conscious, freely moving mice by a telemetry system. We found that saline intake and total fluid intake were significantly reduced in PRRKO mice following DOCA treatment compared with that in wild-type (WT) mice, whereas regular water intake was similar between the genotypes. Sodium preference and total sodium intake were significantly reduced in PRRKO mice compared with WT mice. PRRKO mice also excreted less urine and urinary sodium compared with WT mice following DOCA treatment, whereas potassium excretion was similar between the two groups. Finally, we found that the sodium balance, calculated by subtracting urinary sodium excretion from sodium intake, was greater in WT mice than in PRRKO mice. Collectively, these findings suggest that the neuronal PRR plays a regulatory role in DOCA-induced sodium intake.

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