Differential effects of intravenous hyperosmotic solutes on drinking latency and c-Fos expression in the circumventricular organs and hypothalamus of the rat

2007 ◽  
Vol 292 (4) ◽  
pp. R1690-R1698 ◽  
Author(s):  
Jacqueline M. Ho ◽  
Dannielle K. Zierath ◽  
Anna V. Savos ◽  
Dominic J. Femiano ◽  
John E. Bassett ◽  
...  

Hyperosmotic intravenous infusions of NaCl are more potent for inducing drinking and vasopressin (AVP) secretion than equally osmotic solutions of glucose or urea. The fact that all three solutes increased cerebrospinal fluid osmolality and sodium concentration led the investigators to conclude that critical sodium receptors or osmoreceptors for stimulating drinking and AVP secretion were outside the blood-brain barrier (BBB) in the circumventricular organs (CVOs). We tested an obvious prediction of this hypothesis: that all three solutes should increase c-Fos-like immunoreactivity (Fos-ir) inside the BBB, but that only NaCl should increase Fos-ir in the CVOs. We gave intravenous infusions of 3.0 Osm/l NaCl, glucose, or urea to rats for 11 or 22 min at 0.14 ml/min and perfused the rats for assay of Fos-ir at 90 min. Controls received isotonic NaCl at the same volume. Drinking latency was measured, but water was then removed. Drinking consistently occurred with short latency during hyperosmotic NaCl infusions only. Fos-ir in the forebrain CVOs, the subfornical organ, and organum vasculosum laminae terminalis was consistently elevated only by hyperosmotic NaCl. However, all three hyperosmotic solutes potently stimulated Fos-ir in the supraoptic and paraventricular nuclei of the hypothalamus inside the BBB. Hyperosmotic NaCl greatly elevated Fos-ir in the area postrema, but even glucose and urea caused moderate elevations that may be related to volume expansion rather than osmolality. The data provide strong support for the conclusion that the osmoreceptors controlling drinking are located in the CVOs.

2013 ◽  
Vol 305 (10) ◽  
pp. R1141-R1152 ◽  
Author(s):  
Rebecca L. Miller ◽  
Michelle H. Wang ◽  
Paul A. Gray ◽  
Lawrence B. Salkoff ◽  
Arthur D. Loewy

The sensory circumventricular organs (CVOs) are specialized collections of neurons and glia that lie in the midline of the third and fourth ventricles of the brain, lack a blood-brain barrier, and function as chemosensors, sampling both the cerebrospinal fluid and plasma. These structures, which include the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), and area postrema (AP), are sensitive to changes in sodium concentration but the cellular mechanisms involved remain unknown. Epithelial sodium channel (ENaC)-expressing neurons of the CVOs may be involved in this process. Here we demonstrate with immunohistochemical and in situ hybridization methods that ENaC-expressing neurons are densely concentrated in the sensory CVOs. These neurons become c-Fos activated, a marker for neuronal activity, after various manipulations of peripheral levels of sodium including systemic injections with hypertonic saline, dietary sodium deprivation, and sodium repletion after prolonged sodium deprivation. The increases seen c-Fos activity in the CVOs were correlated with parallel increases in plasma sodium levels. Since ENaCs play a central role in sodium reabsorption in kidney and other epithelia, we present a hypothesis here suggesting that these channels may also serve a related function in the CVOs. ENaCs could be a significant factor in modulating CVO neuronal activity by controlling the magnitude of sodium permeability in neurons. Hence, some of the same circulating hormones controlling ENaC expression in kidney, such as angiotensin II and atrial natriuretic peptide, may coordinate ENaC expression in sensory CVO neurons and could potentially orchestrate sodium appetite, osmoregulation, and vasomotor sympathetic drive.


Neurosurgery ◽  
2013 ◽  
Vol 72 (5) ◽  
pp. 855-860 ◽  
Author(s):  
Pierluigi Longatti ◽  
Luca Basaldella ◽  
Francesco Sammartino ◽  
Alessandro Boaro ◽  
Alessandro Fiorindi

Abstract BACKGROUND: Fluorescein enhancement to detect retinal disorder or differentiate cancer tissue in situ is a well-defined diagnostic procedure. It is a visible marker of where the blood-brain barrier is absent or disrupted. Little is reported in the contemporary literature on endoscopic fluorescein-enhanced visualization of the circumventricular organs, and the relevance of these structures as additional markers for safe ventricular endoscopic navigation remains an unexplored field. OBJECTIVE: To describe fluorescein sodium–enhanced visualization of circumventricular organs as additional anatomic landmarks during endoscopic ventricular surgery procedures. METHODS: We prospectively administered intravenously 500 mg fluorescein sodium in 12 consecutive endoscopic surgery patients. A flexible endoscope equipped with dual observation modes for both white light and fluorescence was used. During navigation from the lateral to the fourth ventricle, the endoscopic anatomic landmarks were first inspected under white light and then under the fluorescent mode. RESULTS: After a mean of 20 seconds in the fluorescent mode, the fluorescein enhanced visualization of the choroid plexus of the lateral ventricle, median eminence–tuber cinereum complex, organum vasculosum of the lamina terminalis, choroid plexus of the third and fourth ventricles, and area postrema. CONCLUSION: Fluorescein-enhanced visualization is a useful tool for helping neuroendoscopists recognize endoscopic anatomic landmarks. It could be adopted to guide orientation when the surgeon deems an endoscopic procedure unsafe or contraindicated because of unclear or subverted anatomic landmarks. Visualization of the circumventricular organs could add new insight into the functional anatomy of these structures, with possible implications for the site and safety of third ventriculostomy.


2001 ◽  
Vol 280 (2) ◽  
pp. E349-E356 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen

Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study assessed the role of the paraventricular nuclei (PVN) in these actions. Intracerebroventricular ET-1 (10 pmol) or the ETA antagonist BQ-123 (40 nmol) was administered in conscious intact or sinoaortic-denervated (SAD) Long-Evans rats with sham or bilateral electrolytic lesions of the magnocellular region of the PVN. Baseline values did not differ among groups, and artificial cerebrospinal fluid (CSF) induced no significant changes. In sham-lesioned rats, ET-1 increased mean arterial pressure (MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD ( P < 0.001 ET-1 vs. CSF) rats. PVN lesions abolished the rise in MAP: −0.1 ± 2.8 mmHg in intact and 0.0 ± 2.9 mmHg in SAD. AVP increased in only in the sham-lesioned SAD group 8.6 ± 3.5 pg/ml ( P < 0.001 ET-1 vs. CSF). BQ-123 blocked the responses. Thus the integrity of the PVN is required for intracerebroventricularly administered ET-1 to exert pressor and AVP secretory effects.


2013 ◽  
Vol 521 (15) ◽  
pp. 3389-3405 ◽  
Author(s):  
Fanny Langlet ◽  
Amandine Mullier ◽  
Sebastien G. Bouret ◽  
Vincent Prevot ◽  
Benedicte Dehouck

2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  

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.


1990 ◽  
Vol 258 (1) ◽  
pp. R57-R63 ◽  
Author(s):  
J. Brown ◽  
A. Czarnecki

Displacement of bound 125I-labeled atrial natriuretic peptide-(1-28) [alpha 125I-ANP-(1-28)] by alpha-ANP-(5-28) and porcine brain natriuretic peptide (BNP) was used to map receptors common to these peptides in rat brain by in vitro autoradiography. alpha-125I-ANP bound reversibly to subfornical organ, area postrema, median preoptic, supraoptic and paraventricular nuclei, and arachnoid mater. Binding at these sites was displaced similarly by 1 microM unlabeled alpha-ANP, alpha-ANP-(5-28), and BNP. Binding dissociation constants in the subfornical organ and arachnoid were 4.40 +/- 1.15 and 3.99 +/- 0.86 nM, respectively, for alpha-ANP, and 2.41 +/- 1.11 and 2.23 +/- 1.06 nM, respectively, for BNP. alpha-125I-ANP also bound to choroid plexus. Here 1 microM unlabeled alpha-ANP displaced significantly more radioligand than did 1 microM BNP, and the concentration displacing 50% of bound radioligand was 2.23 +/- 0.78 nM for alpha-ANP and 1.51 +/- 0.67 nM for BNP. alpha-ANP-(5-28) also displaced alpha 125I-ANP at all sites with significantly greater affinity than did unlabeled alpha-ANP. alpha-125I-ANP was not displaced by completely unrelated peptides. Therefore, both atrial and brain natriuretic peptides may be high-affinity ligands at common receptors in some cerebral localities.


1999 ◽  
Vol 277 (2) ◽  
pp. R532-R540 ◽  
Author(s):  
Kathleen S. Curtis ◽  
J. Thomas Cunningham ◽  
Cheryl M. Heesch

Fos and dopamine β-hydroxylase immunoreactivity were evaluated in the brain stems of 21-day pregnant and virgin female rats injected with either hydralazine (HDZ; 10 mg/kg iv) or vehicle. HDZ produced significant hypotension in both groups, although baseline blood pressure was lower in pregnant rats (96 ± 2.5 mmHg) than in virgin female rats (121 ± 2.8 mmHg). There were no differences in Fos immunoreactivity in the brain stems of pregnant and virgin female rats after vehicle treatment. HDZ-induced hypotension significantly increased Fos expression in both groups; however, the magnitude of the increases differed in the caudal ventrolateral medulla (CVL), the area postrema (AP), and the rostral ventrolateral medulla (RVL). Fos expression after HDZ in pregnant rats was augmented in noncatecholaminergic neurons of the CVL but was attenuated in the AP and in noncatecholaminergic neurons in the RVL. These results are consistent with differences in the sympathetic response to hypotension between pregnant and virgin female rats and indicate that the central response to hypotension may be different in pregnant rats.


1992 ◽  
Vol 262 (3) ◽  
pp. F513-F516 ◽  
Author(s):  
C. Emmeluth ◽  
C. Drummer ◽  
R. Gerzer ◽  
P. Bie

Effects on renal function of an increase in the concentration of sodium in the blood supplying the head were investigated in water-diuretic conscious dogs in which the sodium and water contents were controlled by separate servo-mechanisms. A selective 2% increase in the sodium concentration of the carotid blood was achieved by a split-infusion technique including infusions of hypertonic saline into both carotid arteries and water into a jugular vein at rates making the combined infusate isotonic. This procedure caused a 34-fold increase in renal sodium excretion concomitant with a fourfold increase in the rate of urinary excretion of urodilatin. A comparable isotonic volume expansion (isotonic saline infusion into carotid arteries and jugular vein) caused a significantly smaller (13-fold) increase in urinary rate of excretion of sodium (P less than 0.02) and no increase at all in the excretion of urodilatin. It is hypothesized that cephalic sodium concentration receptors regulate the rate of excretion of sodium via urodilatin even under the present slightly hypotonic conditions.


2003 ◽  
Vol 285 (6) ◽  
pp. R1331-R1339 ◽  
Author(s):  
Douglas A. Fitts ◽  
Simon N. Thornton ◽  
Alexandra A. Ruhf ◽  
Dannielle K. Zierath ◽  
Alan Kim Johnson ◽  
...  

Central injection of ANG II has been proposed to have dual effects on salt appetite including a direct stimulatory effect and an indirect inhibitory effect through an activation of central oxytocinergic neurons. The inhibition was demonstrated by pretreating rats with central ornithine vasotocin (OVT; oxytocin antagonist) 30 min before a central ANG II injection. The OVT pretreatment produced a large increase in ANG II-induced saline intake. The present paper reports a failure to replicate that influential experiment. However, we also report for the first time that OVT by itself: 1) provokes drinking of both water and saline solution with a latency almost as short as that produced by ANG II; 2) produces a mild pressor response; and 3) increases c-Fos expression in the organum vasculosum laminae terminalis (OVLT) and the median preoptic nucleus (MnPO). Oxytocin activity may provide an inhibitory control of drinking responses as has been suggested, but the inhibition is tonic and includes both water and saline drinking. Inhibition of this tonic activity may stimulate drinking by increasing neural activity in the OVLT and MnPO.


Sign in / Sign up

Export Citation Format

Share Document