The periventricular anteroventral third ventricle (AV3V): Its relationship with the subfornical organ and neural systems involved in maintaining body fluid homeostasis

1985 ◽  
Vol 15 (6) ◽  
pp. 595-601 ◽  
Author(s):  
Alan Kim Johnson
Keyword(s):  
Body Fluid ◽  
Third Ventricle ◽  
Subfornical Organ ◽  
Neural Systems ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II

2012 ◽  
Vol 303 (9) ◽  
pp. R921-R928 ◽  
Author(s):  
Jason M. Moreau ◽  
Waseem Iqbal ◽  
Jeffrey K. Turner ◽  
Graham F. Wagner ◽  
John Ciriello
Keyword(s):  
Western Blot ◽  
Water Intake ◽  
Body Fluid ◽  
Physiological Role ◽  
Subfornical Organ ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Glycoprotein Hormone ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

Recently, receptors for the calcium-regulating glycoprotein hormone stanniocalcin-1 (STC-1) have been found within subfornical organ (SFO), a central structure involved in the regulation of electrolyte and body fluid homeostasis. However, whether SFO neurons produce STC-1 and how STC-1 may function in fluid homeostasis are not known. Two series of experiments were done in Sprague-Dawley rats to investigate whether STC-1 is expressed within SFO and whether it exerts an effect on water intake. In the first series, experiments were done to determine whether STC-1 was expressed within cells in SFO using immunohistochemistry, and whether protein and gene expression for STC-1 existed in SFO using Western blot and quantitative RT-PCR, respectively. Cells containing STC-1 immunoreactivity were found throughout the rostrocaudal extent of SFO. STC-1 protein expression within SFO was confirmed with Western blot, and SFO was also found to express STC-1 mRNA. In the second series, microinjections (200 nl) of STC-1, ANG II, a combination of the two or the vehicle were made into SFO in conscious, unrestrained rats. Water intake was measured at 0700 for a 1-h period after each injection in animals. Microinjections of STC-1 (17.6 or 176 nM) alone had no effect on water intake compared with controls. However, STC-1 not only attenuated the drinking responses to ANG II for about 30 min, but also decreased the total water intake over the 1-h period. These data suggest that STC-1 within the SFO may act in a paracrine/autocrine manner to modulate the neuronal responses to blood-borne ANG II. These findings also provide the first direct evidence of a physiological role for STC-1 in central regulation of body fluid homeostasis.

Functional relationship between subfornical organ cholinergic stimulation and nitrergic activation influencing cardiovascular and body fluid homeostasis

2007 ◽  
Vol 143 (1-3) ◽  
pp. 28-33 ◽  
Author(s):  
Wilson Abrão Saad ◽  
Ismael Francisco Motta Siqueira Guarda ◽  
Luis Antonio de Arruda Camargo ◽  
Talmir Augusto Faria Brisola dos Santos ◽  
William Abrão Saad
Keyword(s):  
Body Fluid ◽  
Functional Relationship ◽  
Subfornical Organ ◽  
Cholinergic Stimulation ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

scholarly journals DREADD-induced activation of subfornical organ neurons stimulates thirst and salt appetite

2016 ◽  
Vol 115 (6) ◽  
pp. 3123-3129 ◽  
Author(s):  
Haley L. Nation ◽  
Marvin Nicoleau ◽  
Brian J. Kinsman ◽  
Kirsteen N. Browning ◽  
Sean D. Stocker
Keyword(s):  
Water Intake ◽  
Body Fluid ◽  
Subfornical Organ ◽  
Designer Drugs ◽  
Salt Appetite ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis ◽  
Acute Injection

The subfornical organ (SFO) plays a pivotal role in body fluid homeostasis through its ability to integrate neurohumoral signals and subsequently alter behavior, neuroendocrine function, and autonomic outflow. The purpose of the present study was to evaluate whether selective activation of SFO neurons using virally mediated expression of Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) stimulated thirst and salt appetite. Male C57BL/6 mice (12–15 wk) received an injection of rAAV2-CaMKII-HA-hM3D(Gq)-IRES-mCitrine targeted at the SFO. Two weeks later, acute injection of clozapine N-oxide (CNO) produced dose-dependent increases in water intake of mice with DREADD expression in the SFO. CNO also stimulated the ingestion of 0.3 M NaCl. Acute injection of CNO significantly increased the number of Fos-positive nuclei in the SFO of mice with robust DREADD expression. Furthermore, in vivo single-unit recordings demonstrate that CNO significantly increases the discharge frequency of both ANG II- and NaCl-responsive neurons. In vitro current-clamp recordings confirm that bath application of CNO produces a significant membrane depolarization and increase in action potential frequency. In a final set of experiments, chronic administration of CNO approximately doubled 24-h water intake without an effect on salt appetite. These findings demonstrate that DREADD-induced activation of SFO neurons stimulates thirst and that DREADDs are a useful tool to acutely or chronically manipulate neuronal circuits influencing body fluid homeostasis.

Neuroendocrine Control of Body Fluid Metabolism

2004 ◽  
Vol 84 (1) ◽  
pp. 169-208 ◽  
Author(s):  
JOSÉ ANTUNES-RODRIGUES ◽  
MARGARET DE CASTRO ◽  
LUCILA L. K. ELIAS ◽  
MARCELO M. VALENÇA ◽  
SAMUEL M. McCANN
Keyword(s):  
Body Fluid ◽  
Defense Mechanism ◽  
Third Ventricle ◽  
Extracellular Fluid ◽  
Volume Overload ◽  
Body Fluids ◽  
Potent Inducer ◽  
Neuroendocrine Control ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis

Antunes-Rodrigues, José, Margaret de Castro, Lucila L. K. Elias, Marcelo M. Valença, and Samuel M. McCann. Neuroendocrine Control of Body Fluid Metabolism. Physiol Rev 84: 169–208, 2004; 10.1152/physrev.00017.2003.—Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in bodyfluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

Physiological regulation of the renal vasopressin receptor-effector pathway in dogs

1990 ◽  
Vol 258 (3) ◽  
pp. R763-R769
Author(s):  
L. B. Kinter ◽  
N. Caldwell ◽  
S. Caltabiano ◽  
C. Winslow ◽  
D. P. Brooks ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Body Fluid ◽  
Physiological State ◽  
Extracellular Volume ◽  
Conscious Dogs ◽  
Physiological Regulation ◽  
Fluid Homeostasis ◽  
Effector Pathway ◽  
Body Fluid Homeostasis ◽  
V2 Receptor

Physiological regulation of receptor-effector pathways is recognized as a significant factor determining target organ selectivity and sensitivity in several hormonal systems. Whether or not physiological regulation of the renal vasopressin (V2) receptor-effector pathway participates in the control of body fluid homeostasis is unknown. We evaluated four states likely to be associated with altered sensitivities of the renal V2 receptor-effector pathway as follows: dehydration (18-h hydropenia), volume expansion, exogenous arginine vasopressin (AVP) infusion (10 ng/kg + 0.25 ng.kg-1.h-1), and cyclooxygenase blockade (indomethacin, 2 mg/kg + 2 mg.kg-1.h-1) for effects on the antidiuretic efficacies and potencies of putative V2-receptor antagonists in conscious dogs. The antidiuretic efficacies of desGly9[Pmp1-D-Tyr(Et)2Val4]AVP [Smith Kline & French (SK&F) 101926; 0.01-1,000 micrograms/kg] ranged from that of a full agonist to that of an antagonist, depending on the physiological state studied. The vasopressin antagonist potency of SK&F 101926 was increased 150-fold in association with extracellular volume expansion and decreased by blockade of renal cyclooxygenase activity. This spectrum of activities is that anticipated for a partial agonist under conditions where receptor number and/or sensitivity of receptor-effector coupling is increased or decreased, respectively. Thus volume expansion and increased circulating vasopressin concentration are associated with effective decreases, whereas hydropenia and cyclooxygenase blockade are associated with effective increases in sensitivity of the renal V2 receptor-effector pathway in the dog kidney. We conclude that the V2 receptor-effector pathway is a site of integration of physiological mechanisms participating in the control of body fluid homeostasis in conscious dogs.

Sign in / Sign up

Export Citation Format

Share Document