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.

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.

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.

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.

Fluorescein-Enhanced Characterization of Additional Anatomical Landmarks in Cerebral Ventricular Endoscopy

Neurosurgery ◽  
2013 ◽  
Vol 72 (5) ◽  
pp. 855-860 ◽  
Author(s):  
Pierluigi Longatti ◽  
Luca Basaldella ◽  
Francesco Sammartino ◽  
Alessandro Boaro ◽  
Alessandro Fiorindi
Keyword(s):  
Choroid Plexus ◽  
White Light ◽  
Area Postrema ◽  
Functional Anatomy ◽  
Circumventricular Organs ◽  
Third Ventriculostomy ◽  
Cancer Tissue ◽  
Anatomical Landmarks ◽  
Fluorescein Sodium ◽  
Anatomic Landmarks

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.

scholarly journals Sulprostone-Induced Gastric Dysrhythmia in the Ferret: Conventional and Advanced Analytical Approaches

2021 ◽  
Vol 11 ◽  
Author(s):  
Zengbing Lu ◽  
Yu Zhou ◽  
Longlong Tu ◽  
Sze Wa Chan ◽  
Man P. Ngan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Analytical Techniques ◽  
Dominant Frequency ◽  
Fluctuation Analysis ◽  
Prostaglandin E ◽  
Myoelectric Activity ◽  
Core Body ◽  
Analytical Approaches

Nausea and emesis resulting from disease or drug treatment may be associated with disrupted gastric myoelectric activity (GMA). Conventional analytical techniques can determine the relative degrees of brady-, normo-, and tachygastric power, but lose information relative to the basic slow wave shape. The aim of the present study was to investigate the application of advanced analytical techniques in the analysis of disrupted GMA recorded after administration of sulprostone, a prostaglandin E3/1 agonist, in ferrets. Ferrets were implanted with radiotelemetry devices to record GMA, blood pressure, heart rate (HR) and core body temperature 1 week before the administration of sulprostone (30 μg/kg) or vehicle (saline, 0.5 mL/kg). GMA was initially analyzed using fast Fourier transformations (FFTs) and a conventional power partitioning. Detrended fluctuation analysis (DFA) was also applied to the GMA recordings to reveal information relative to the fluctuation of signals around local trends. Sample entropy (SampEn) analysis was used for examining the regularity of signals. Conventional signal processing techniques revealed that sulprostone increased the dominant frequency (DF) of slow waves, with an increase in the percentage power of the tachygastric range and a decrease in the percentage power of the normogastric range. DFA revealed that sulprostone decreased the fluctuation function, indicative of a loss of the variability of GMA fluctuations around local trends. Sulprostone increased SampEn values, indicating a loss of regularity in the GMA data. Behaviorally, sulprostone induced emesis and caused defecation. It also increased blood pressure and elevated HR, with an associated decrease in HR variability (HRV). Further analysis of HRV revealed a decrease in both low-frequency (LF) and high-frequency (HF) components, with an overall increase in the LF/HF ratio. Sulprostone did not affect core body temperature. In conclusion, DFA and SampEn permit a detailed analysis of GMA, which is necessary to understand the action of sulprostone to modulate gastric function. The action to decrease HRV and increase the LF/HF ratio may be consistent with a shift toward sympathetic nervous system dominance, commonly seen during nausea.

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.

Sodium depletion induces Fos immunoreactivity in circumventricular organs of the lamina terminalis

1995 ◽  
Vol 679 (1) ◽  
pp. 34-41 ◽  
Author(s):  
Laura Vivas ◽  
Cinthia Veronica Pastuskovas ◽  
Leonardo Tonelli
Keyword(s):  
Circumventricular Organs ◽  
Lamina Terminalis ◽  
Sodium Depletion

scholarly journals Neural Mechanisms of Inflammation-Induced Fever

2018 ◽  
Vol 24 (4) ◽  
pp. 381-399 ◽  
Author(s):  
Anders Blomqvist ◽  
David Engblom
Keyword(s):  
Peripheral Nerves ◽  
Circumventricular Organs ◽  
Neural Mechanisms ◽  
Prostaglandin E ◽  
Receptor Subtype ◽  
Common Symptom ◽  
Immune Challenge ◽  
Brain Endothelial Cells ◽  
Efferent Limb ◽  
The Brain

Fever is a common symptom of infectious and inflammatory disease. It is well-established that prostaglandin E2 is the final mediator of fever, which by binding to its EP3 receptor subtype in the preoptic hypothalamus initiates thermogenesis. Here, we review the different hypotheses on how the presence of peripherally released pyrogenic substances can be signaled to the brain to elicit fever. We conclude that there is unequivocal evidence for a humoral signaling pathway by which proinflammatory cytokines, through their binding to receptors on brain endothelial cells, evoke fever by eliciting prostaglandin E2 synthesis in these cells. The evidence for a role for other signaling routes for fever, such as signaling via circumventricular organs and peripheral nerves, as well as transfer into the brain of peripherally synthesized prostaglandin E2 are yet far from conclusive. We also review the efferent limb of the pyrogenic pathways. We conclude that it is well established that prostaglandin E2 binding in the preoptic hypothalamus produces fever by disinhibition of presympathetic neurons in the brain stem, but there is yet little understanding of the mechanisms by which factors such as nutritional status and ambient temperature shape the response to the peripheral immune challenge.

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