scholarly journals Tanycyte-like cells form a blood-cerebrospinal fluid barrier in the circumventricular organs of the mouse brain

2013 ◽  
Vol 521 (15) ◽  
pp. 3389-3405 ◽  
Author(s):  
Fanny Langlet ◽  
Amandine Mullier ◽  
Sebastien G. Bouret ◽  
Vincent Prevot ◽  
Benedicte Dehouck
Keyword(s):  
Cerebrospinal Fluid ◽  
Mouse Brain ◽  
Circumventricular Organs

scholarly journals Tanycyte-like cells form a blood-cerebrospinal fluid barrier in the circumventricular organs of the mouse brain

2013 ◽  
Vol 521 (15) ◽  
pp. spc1-spc1 ◽  
Author(s):  
Fanny Langlet ◽  
Amandine Mullier ◽  
Sebastien G. Bouret ◽  
Vincent Prevot ◽  
Benedicte Dehouck
Keyword(s):  
Cerebrospinal Fluid ◽  
Mouse Brain ◽  
Circumventricular Organs

scholarly journals Embryonic Cerebrospinal Fluid Activates Neurogenesis of Neural Precursors within the Subventricular Zone of the Adult Mouse Brain

2013 ◽  
Vol 198 (5) ◽  
pp. 398-404 ◽  
Author(s):  
E. Carnicero ◽  
M.I. Alonso ◽  
R. Carretero ◽  
F. Lamus ◽  
J.A. Moro ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Mouse Brain ◽  
Subventricular Zone ◽  
Adult Mouse ◽  
Adult Mouse Brain ◽  
Neural Precursors

scholarly journals Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid

2012 ◽  
Vol 02 (02) ◽  
pp. 68-73 ◽  
Author(s):  
Emilia M. Carmona-Calero ◽  
Ibrahim González-Marrero ◽  
Manuela Castañeyra-Martin ◽  
Juan M. González-Toledo ◽  
Leandro Castañeyra-Ruiz ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Circumventricular Organs

scholarly journals How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension

2012 ◽  
Vol 302 (5) ◽  
pp. H1031-H1049 ◽  
Author(s):  
Mordecai P. Blaustein ◽  
Frans H. H. Leenen ◽  
Ling Chen ◽  
Vera A. Golovina ◽  
John M. Hamlyn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Signaling Pathway ◽  
Vascular Resistance ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Dietary Salt ◽  
New Paradigm

Excess dietary salt is a major cause of hypertension. Nevertheless, the specific mechanisms by which salt increases arterial constriction and peripheral vascular resistance, and thereby raises blood pressure (BP), are poorly understood. Here we summarize recent evidence that defines specific molecular links between Na+ and the elevated vascular resistance that directly produces high BP. In this new paradigm, high dietary salt raises cerebrospinal fluid [Na+]. This leads, via the Na+-sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction. Plasma levels of endogenous ouabain (EO), the Na+ pump ligand, also become elevated. Remarkably, high cerebrospinal fluid [Na+]-evoked, locally secreted (hypothalamic) EO participates in a pathway that mediates the sustained increase in SNA. This hypothalamic signaling chain includes aldosterone, epithelial Na+ channels, EO, ouabain-sensitive α2 Na+ pumps, and angiotensin II (ANG II). The EO increases (e.g.) hypothalamic ANG-II type-1 receptor and NADPH oxidase and decreases neuronal nitric oxide synthase protein expression. The aldosterone-epithelial Na+ channel-EO-α2 Na+ pump-ANG-II pathway modulates the activity of brain cardiovascular control centers that regulate the BP set point and induce sustained changes in SNA. In the periphery, the EO secreted by the adrenal cortex directly enhances vasoconstriction via an EO-α2 Na+ pump-Na+/Ca2+ exchanger-Ca2+ signaling pathway. Circulating EO also activates an EO-α2 Na+ pump-Src kinase signaling cascade. This increases the expression of the Na+/Ca2+ exchanger-transient receptor potential cation channel Ca2+ signaling pathway in arterial smooth muscle but decreases the expression of endothelial vasodilator mechanisms. Additionally, EO is a growth factor and may directly participate in the arterial structural remodeling and lumen narrowing that is frequently observed in established hypertension. These several central and peripheral mechanisms are coordinated, in part by EO, to effect and maintain the salt-induced elevation of BP.

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.

Transportin 1 in the mouse brain: Appearance in regions of neurogenesis, cerebrospinal fluid production/sensing, and circadian clock

2011 ◽  
Vol 519 (9) ◽  
pp. 1770-1780 ◽  
Author(s):  
Miho Sato ◽  
Yasutaka Mizoro ◽  
Yuta Atobe ◽  
Yoshito Fujimoto ◽  
Yoshiaki Yamaguchi ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Circadian Clock ◽  
Mouse Brain ◽  
Fluid Production

Uptake of Exogenous Aspartate into Circumventricular Organs but Not Other Regions of Adult Mouse Brain

1984 ◽  
Vol 42 (3) ◽  
pp. 740-744 ◽  
Author(s):  
Madelon T. Price ◽  
Mary Ellen Pusateri ◽  
Sue Ella Crow ◽  
Susan Buchsbaum ◽  
John W. Olney ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Circumventricular Organs ◽  
Adult Mouse Brain
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