The functional and structural border between the CSF-and blood-milieu in the circumventricular organs (organum vasculosum laminae terminalis, subfornical organ, area postrema) of the rat

1978 ◽  
Vol 195 (3) ◽  
Author(s):  
B. Krisch ◽  
H. Leonhardt ◽  
W. Buchheim
Keyword(s):  
Area Postrema ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Organum Vasculosum Laminae Terminalis ◽  
Organum Vasculosum

Increases in brain and cardiac AT1 receptor and ACE densities after myocardial infarct in rats

2004 ◽  
Vol 286 (5) ◽  
pp. H1665-H1671 ◽  
Author(s):  
Junhui Tan ◽  
Hao Wang ◽  
Frans H. H. Leenen
Keyword(s):  
Paraventricular Nucleus ◽  
Receptor Binding ◽  
Myocardial Infarct ◽  
Subfornical Organ ◽  
Preoptic Nucleus ◽  
Fab Fragments ◽  
Intracerebroventricular Infusion ◽  
Organum Vasculosum Laminae Terminalis ◽  
Organum Vasculosum ◽  
The Brain

In the brain, ouabain-like compounds (OLC) and the reninangiotensin system (RAS) contribute to sympathetic hyperactivity in rats after myocardial infarction (MI). This study aimed to evaluate changes in components of the central vs. the peripheral RAS. Angiotensin-converting enzyme (ACE) and angiotensin type 1 (AT1) receptor binding densities were determined by measuring 125I-labeled 351A and 125I-labeled ANG II binding 4 and 8 wk after MI. In the brain, ACE and AT1 receptor binding increased 8–15% in the subfornical organ, 14–22% in the organum vasculosum laminae terminalis, 20–34% in the paraventricular nucleus, and 13–15% in the median preoptic nucleus. In the heart, the greatest increase in ACE and AT1 receptor binding occurred at the infarct scar (∼10-fold) and the least in the right ventricle (2-fold). In kidneys, ACE and AT1 receptor binding decreased 10–15%. After intracerebroventricular infusion of Fab fragments to block brain OLC from 0.5 to 4 wk after MI, increases in ACE and AT1 receptors in the subfornical organ, organum vasculosum laminae terminalis, paraventricular nucleus, and medial preoptic nucleus were markedly inhibited, and ACE and AT1 receptor densities in the heart increased less (6-fold in the infarct scar). In kidneys, decreases in ACE and AT1 receptor binding were absent after treatment with Fab fragments. These results demonstrate that ACE and AT1 receptor binding densities increase not only in the heart but also in relevant areas of the brain of rats after MI. Brain OLC appears to play a major role in activation of brain RAS in rats after MI and, to a modest degree, in activation of the cardiac RAS.

Subfornical organ disconnection alters Fos expression in the lamina terminalis, supraoptic nucleus, and area postrema after intragastric hypertonic NaCl

2005 ◽  
Vol 288 (4) ◽  
pp. R947-R955 ◽  
Author(s):  
Julia A. Freece ◽  
Julie E. Van Bebber ◽  
Dannielle K. Zierath ◽  
Douglas A. Fitts
Keyword(s):  
Supraoptic Nucleus ◽  
Area Postrema ◽  
Anterior Commissure ◽  
Subfornical Organ ◽  
Main Body ◽  
Lamina Terminalis ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Organum Vasculosum Laminae Terminalis ◽  
Initial Load

The lamina terminalis was severed by a horizontal knife cut through the anterior commissure to determine the effects of a disconnection of the subfornical organ (SFO) on drinking and Fos-like immunoreactivity (Fos-ir) in the rat brain in response to an intragastric load of hypertonic saline (5 ml/kg of 1.5 M NaCl by gavage). After an initial load, knife-cut rats drank significantly less water than sham-cut rats, thus confirming a role for the SFO in osmotic drinking. After a second load at least 1 wk later, the rats were not allowed to drink after the gavage and were perfused for analysis of Fos-ir at 90 min. Compared with sham-cut rats, the knife-cut rats displayed significantly elevated Fos-ir in the main body of the SFO, in the dorsal cap of the organum vasculosum laminae terminalis, and in the ventral median preoptic nucleus after the hypertonic load. The knife cut significantly decreased Fos-ir in the supraoptic nucleus. Fos-ir was expressed mainly in the midcoronal and caudal parts of the area postrema of sham-cut rats, and this expression was greatly reduced in knife-cut rats. These findings strengthen the case for the presence of independently functioning osmoreceptors within the SFO and suggest that the structures of the lamina terminalis provide mutual inhibition during hypernatremia. They also demonstrate that the Fos-ir in the area postrema after intragastric osmotic loading is heavily dependent on the intact connectivity of the SFO.

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 ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Volume Expansion ◽  
Area Postrema ◽  
Strong Support ◽  
Sodium Concentration ◽  
Circumventricular Organs ◽  
Paraventricular Nuclei ◽  
Intravenous Infusions ◽  
Organum Vasculosum Laminae Terminalis ◽  
Fos Expression

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.

Lesions of area postrema and subfornical organ alter exendin-4-induced brain activation without preventing the hypophagic effect of the GLP-1 receptor agonist

2010 ◽  
Vol 298 (4) ◽  
pp. R1098-R1110 ◽  
Author(s):  
Elena-Dana Baraboi ◽  
Pauline Smith ◽  
Alastair V. Ferguson ◽  
Denis Richard
Keyword(s):  
Area Postrema ◽  
Brain Structures ◽  
Circumventricular Organs ◽  
Primary Objective ◽  
Subfornical Organ ◽  
Metabolic Effects ◽  
Ventrolateral Medulla ◽  
Hypothalamic Nucleus ◽  
Medial Nucleus ◽  
Electrolytic Ablation

The mechanism and route whereby glucagon-like peptide 1 (GLP-1) receptor agonists, such as GLP-1 and exendin-4 (Ex-4), access the central nervous system (CNS) to exert their metabolic effects have yet to be clarified. The primary objective of the present study was to investigate the potential role of two circumventricular organs (CVOs), the area postrema (AP) and the subfornical organ (SFO), in mediating the metabolic and CNS-stimulating effects of Ex-4. We demonstrated that electrolytic ablation of the AP, SFO, or AP + SFO does not acutely prevent the anorectic effects of Ex-4. AP + SFO lesion chronically decreased food intake and body weight and also modulated the effect of Ex-4 on the neuronal activation of brain structures involved in the hypothalamic-pituitary-adrenal axis and glucose metabolism. The results of the study also showed that CVO lesions blunted Ex-4-induced expression of c- fos mRNA (a widely used neuronal activity marker) in 1) limbic structures (bed nucleus of the stria terminalis and central amygdala), 2) hypothalamus (paraventricular hypothalamic nucleus, supraoptic nucleus, and arcuate nucleus), and 3) hindbrain (lateral and lateral-external parabrachial nucleus, medial nucleus of the solitary tract, and ventrolateral medulla). In conclusion, although the present results do not support a role for the CVOs in the anorectic effect induced by a single injection of Ex-4, they suggest that the CVOs play important roles in mediating the actions of Ex-4 in the activation of CNS structures involved in homeostatic control.

Central actions of angiotensin in cardiovascular control: Multiple roles for a single peptide

1992 ◽  
Vol 70 (5) ◽  
pp. 779-785 ◽  
Author(s):  
Alastair V. Ferguson ◽  
Katharine M. Wall
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Cardiovascular Control ◽  
Multiple Roles ◽  
Ang Ii ◽  
Electrophysiological Studies ◽  
The Central Nervous System ◽  
Central Actions

Angiotensin II (ANG II) acts peripherally as a hormone, with actions on the vasculature, adrenals, and kidney. In addition, certain actions of ANG II in the central nervous system are directed toward cardiovascular control and fluid volume homeostasis. Dense binding sites for ANG II are found at circumventricular organs, which apparently have the ability to relay information to cardiovascular centers via neural circuitry. Microinjection of ANG II into the subfornical organ (SFO) or area postrema (AP) produces site-specific increases in blood pressure. In addition, electrophysiological studies demonstrate profound effects of ANG II, acting at the SFO, on activity of neurohypophysial neurons and release of oxytocin and vasopressin, which can be antagonized by ANG II blockers or attenuated by SFO lesions. Evidence from microinjection, electrophysiological, and lesion studies indicate a complex interaction between central sites involved in mechanisms of cardiovascular control: the SFO, AP, organum vasculosum of the lamina terminalis, and paraventricular and supraoptic nuclei of the hypothalamus. Not only is ANG II a humoral messenger in this central scenario, but evidence suggests it acts as a neurotransmitter or neuroendocrine substance within specific CNS pathways, suggesting multiple roles for this peptide in central cardiovascular control.Key words: blood pressure regulation, circumventricular organs, vasopressin, area postrema, subfornical organ.

scholarly journals Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity

2000 ◽  
Vol 279 (6) ◽  
pp. R2277-R2286 ◽  
Author(s):  
Douglas A. Fitts ◽  
Elizabeth M. Starbuck ◽  
Alexandra Ruhf
Keyword(s):  
Blood Pressure ◽  
Water Intake ◽  
Femoral Vein ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Apparent Contradiction ◽  
Organum Vasculosum Laminae Terminalis

A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

Circumventricular organs and fever

1997 ◽  
Vol 273 (5) ◽  
pp. R1690-R1695 ◽  
Author(s):  
Yoshimi Takahashi ◽  
Pauline Smith ◽  
Alistair Ferguson ◽  
Quentin J. Pittman
Keyword(s):  
Body Temperature ◽  
Area Postrema ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Prostaglandin E ◽  
Lamina Terminalis ◽  
Sham Control ◽  
Access Points ◽  
Efferent Projections ◽  
Intravenous Catheters

We have examined the roles of three circumventricular organs, the area postrema, the subfornical organ, and the organum vasculosum of the lamina terminalis (OVLT), as possible access points for circulating pyrogens to cause fever. In conscious, unrestrained rats prepared with telemetry devices, intracerebroventricular cannulas, and intravenous catheters, body temperature was monitored after intravenously administered lipopolysaccharide and, on a different occasion, after intracerebroventricular prostaglandin E1. Lipopolysaccharide-induced fevers in sham control lesioned rats were indistinguishable from those observed in animals with lesions of the area postrema, the OVLT, or the tissue immediately adjacent to this structure (peri-OVLT). In contrast, rats with lesions of the subfornical organ displayed reduced fevers. In none of the groups of lesioned animals were prostaglandin E1 fevers reduced. Thus lesions did not interfere with central thermogenic pathways responsive to prostaglandin. Our results indicate that subfornical organ neurons respond to circulating pyrogens and through their efferent projections activate central pathways involved in fever.

Alterations in atrial natriuretic peptide receptors in rat brain nuclei during hypertension and dehydration

1988 ◽  
Vol 66 (3) ◽  
pp. 288-294 ◽  
Author(s):  
Juan M. Saavedra
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Rat Brain ◽  
Choroid Plexus ◽  
Natriuretic Peptide ◽  
Area Postrema ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Peptide Receptors ◽  
Natriuretic Peptide Receptors ◽  
Atrial Natriuretic

We have studied the localization, kinetics, and regulation of receptors for the circulating form of the atrial natriuretic peptide (99–126) in the rat brain. Atrial natriuretic peptide receptors were discretely localized in the rat brain, with the highest concentrations in circumventricular organs, the choroid plexus, and selected hypothalamic nuclei involved in the production of the antidiuretic hormone vasopressin and in blood pressure control. Spontaneously (genetic) hypertensive rats showed much lower numbers of atrial natriuretic peptide receptors than normotensive controls in the subfornical organ, the area postrema, the nucleus of the solitary tract, and in the choroid plexus. These changes are in contrast with those observed for receptors of angiotensin II, another circulating peptide with actions opposite to those of the atrial natriuretic peptide. In acute dehydration after water deprivation, as well as in chronic dehydration such as that present in homozygous Brattleboro rats, there was an up-regulation of atrial natriuretic peptide receptors in the subfornical organ. Thus, circumventricular organs contain atrial natriuretic peptide receptors that could respond to variations in the concentration of circulating peptide. The localization of atrial natriuretic peptide receptors and the alterations in their regulation present in hypertensive and dehydrated rats indicate that these brain receptors are related to fluid regulation, including the secretion of vasopressin, and to cardiovascular function. Atrial natriuretic peptide receptors in the choroid plexus may be related to the formation of cerebrospinal fluid.

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