scholarly journals Cerebrospinal fluid formation is controlled by membrane transporters to modulate intracranial pressure

2021 ◽  
Author(s):  
Eva K. Oernbo ◽  
Annette B. Steffensen ◽  
Pooya Razzaghi Khamesi ◽  
Trine L. Toft-Bertelsen ◽  
Dagne Barbuskaite ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Choroid Plexus ◽  
Molecular Mechanisms ◽  
Osmotic Gradient ◽  
Pharmaceutical Therapy ◽  
Osmotic Water ◽  
Life Threatening ◽  
Molecular Mode ◽  
Csf Production

AbstractDisturbances in the brain fluid balance can lead to life-threatening elevation in the intracranial pressure (ICP), which represents a vast clinical challenge. Nevertheless, the molecular mechanisms governing cerebrospinal fluid (CSF) secretion are largely unresolved, thus preventing targeted and efficient pharmaceutical therapy of cerebral pathologies involving elevated ICP. Here, we employed experimental rats to demonstrate low osmotic water permeability of the choroid plexus, lack of an osmotic gradient across this tissue, and robust CSF secretion against osmotic gradients. Together, these results illustrate that CSF secretion occurs independently of conventional osmosis, which challenges the existing assumption that CSF production is driven entirely by bulk osmotic forces across the CSF-secreting choroid plexus. Instead, we reveal that the choroidal Na+/K+/Cl− cotransporter NKCC1, Na+/HCO3− cotransporter NBCe2, and Na+/K+-ATPase are actively involved in CSF production and propose a molecular mode of water transport supporting CSF production in this secretory tissue. Further, we demonstrate that inhibition of NKCC1 directly reduces the ICP, illustrating that altered CSF secretion may be employed as a strategy to modulate ICP. These insights identify new promising therapeutic targets against brain pathologies associated with elevated ICP.

Surgical removal of bilateral papillomas of the choroid plexus of the lateral ventricles with resolution of hydrocephalus

1979 ◽  
Vol 50 (5) ◽  
pp. 677-681 ◽  
Author(s):  
Steven K. Gudeman ◽  
Humbert G. Sullivan ◽  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Large Volume ◽  
Surgical Removal ◽  
Tumor Removal ◽  
Content Type ◽  
Lateral Ventricles ◽  
Csf Diversion ◽  
Csf Production ◽  
Fine Print

✓ The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.

Role of NaCl cotransport in cerebrospinal fluid production: effects of loop diuretics

1991 ◽  
Vol 71 (3) ◽  
pp. 795-800 ◽  
Author(s):  
S. Javaheri
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Ionic Composition ◽  
Reasonable Assumption ◽  
Cerebral Ventricles ◽  
Fluid Production ◽  
Production Effects ◽  
Nacl Cotransport ◽  
Csf Production

Cerebrospinal fluid (CSF) is secreted primarily by the choroid plexus (CP) located in the cerebral ventricles. Although much is known about ionic composition of cisternal CSF, the mechanisms involved in secretion of CSF in mammals are still not understood. The main aim of this report is to critically review the role of NaCl cotransport carrier in CSF production. On the basis of the studies in the literature, a model for CSF production by the CP is proposed. In this model, CP cells are assumed to be equipped with an NaCl cotransport carrier located on the basolateral (blood-facing) membrane. Because Na+ and Cl- are the two principal ions in CSF, their continued secretions into cerebral ventricles by CP cells require an adequate intracellular supply, which may be guaranteed by the NaCl cotransport carrier. Although this appears to be a reasonable assumption, making the processes involved in CSF production similar to those of other secretory epithelial cells, the presence of such a carrier in mammalian CP remains controversial. The reasons for this controversy are critically reviewed, and some suggestions for further studies are made.

Reduced cerebrospinal fluid production and intracranial pressure in mice lacking choroid plexus water channel Aquaporin‐1

2004 ◽  
Vol 19 (1) ◽  
pp. 76-78 ◽  
Author(s):  
Kotaro Oshio ◽  
Hiroyuki Watanabe ◽  
Yaunlin Song ◽  
A. S. Verkman ◽  
Geoffrey T. Manley
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Choroid Plexus ◽  
Water Channel ◽  
Aquaporin 1 ◽  
Fluid Production

scholarly journals SOX9-COL9A3–dependent regulation of choroid plexus epithelial polarity governs blood–cerebrospinal fluid barrier integrity

2021 ◽  
Vol 118 (6) ◽  
pp. e2009568118
Author(s):  
Keng Ioi Vong ◽  
Tsz Ching Ma ◽  
Baiying Li ◽  
Thomas Chun Ning Leung ◽  
Wenyan Nong ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Molecular Mechanisms ◽  
Structural Integrity ◽  
Protein Composition ◽  
Transepithelial Transport ◽  
Electrolyte Balance ◽  
Genetic Ablation ◽  
Correct Orientation ◽  
Extracellular Matrix Components

The choroid plexus (CP) is an extensively vascularized neuroepithelial tissue that projects into the brain ventricles. The restriction of transepithelial transport across the CP establishes the blood–cerebrospinal fluid (CSF) barrier that is fundamental to the homeostatic regulation of the central nervous system microenvironment. However, the molecular mechanisms that control this process remain elusive. Here we show that the genetic ablation of Sox9 in the hindbrain CP results in a hyperpermeable blood–CSF barrier that ultimately upsets the CSF electrolyte balance and alters CSF protein composition. Mechanistically, SOX9 is required for the transcriptional up-regulation of Col9a3 in the CP epithelium. The reduction of Col9a3 expression dramatically recapitulates the blood–CSF barrier defects of Sox9 mutants. Loss of collagen IX severely disrupts the structural integrity of the epithelial basement membrane in the CP, leading to progressive loss of extracellular matrix components. Consequently, this perturbs the polarized microtubule dynamics required for correct orientation of apicobasal polarity and thereby impedes tight junction assembly in the CP epithelium. Our findings reveal a pivotal cascade of SOX9-dependent molecular events that is critical for construction of the blood–CSF barrier.

Effect of acetazolamide and furosemide on the production and composition of cerebrospinal fluid from the cat choroid plexus

1982 ◽  
Vol 60 (3) ◽  
pp. 405-409 ◽  
Author(s):  
James M. Melby ◽  
Lewis C. Miner ◽  
Donal J. Reed
Keyword(s):  
Cerebrospinal Fluid ◽  
Drug Treatment ◽  
Choroid Plexus ◽  
Transport Mechanism ◽  
Electrolyte Composition ◽  
K Concentration ◽  
Drug Free ◽  
K Transport ◽  
Csf Production

The effect of acetazolamide and furosemide on choroid plexus (CP) production and electrolyte composition of cerebrospinal fluid (CSF) from the cat CP in situ was investigated. Both drugs decreased CSF production by the CP by 50–90% from a control rate of 0.53 μL ∙ min−1 ∙ mg−1 CP within 1.5–2.5 h after the start of drug treatment. The results were similar whether the drug was administered intravenously or applied directly to the CSF side of the CP. A number of experiments in which the effect of administering drugs via the chamber were studied were continued with the drugs removed by washing the preparation with drug-free artificial CSF and the responses measured. The results demonstrated that the effects of acetazolamide and furosemide were reversed during the 1st h following the washout. Both drugs decreased K concentration of nascent CSF when administered intravenously and furosemide also did so when administered on the CSF side of the CP. It is concluded from these and previous data that acetazolamide and furosemide markedly inhibit the transport mechanism(s) in the cat CP that are responsible for CP secretion which represents about 40–60% of the total CSF production and that K transport is also affected.

Hydrocephalus secondary to diffuse villous hyperplasia of the choroid plexus

1996 ◽  
Vol 85 (4) ◽  
pp. 689-691 ◽  
Author(s):  
Gavin W. Britz ◽  
D. Kyle Kim ◽  
John D. Loeser
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Resonance Imaging ◽  
Ventriculoatrial Shunt ◽  
Content Type ◽  
Tomography Scanning ◽  
Csf Production ◽  
Choroid Plexus Papillomas ◽  
Fine Print

✓ Diffuse villous hyperplasia of the choroid plexus, which is distinct from bilateral choroid plexus papillomas, is extremely rare and is often associated with hydrocephalus due to the overproduction of cerebrospinal fluid (CSF). The authors describe an infant with hydrocephalus, diagnosed by computerized tomography scanning, who developed ascites following placement of a ventriculoperitoneal shunt and, subsequently, demonstrated excessive CSF production when the shunt was externalized. The patient was later successfully treated by placement of a ventriculoatrial shunt. Magnetic resonance imaging demonstrated diffuse villous hyperplasia of the choroid plexus as the cause of the patient's hydrocephalus. The literature on diffuse villous hyperplasia of the choroid plexus is reviewed.

Effect of vasopressin on production of cerebrospinal fluid: possible role of vasopressin (V1)-receptors

1990 ◽  
Vol 258 (1) ◽  
pp. R94-R98 ◽  
Author(s):  
F. M. Faraci ◽  
W. G. Mayhan ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Arginine Vasopressin ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Ventriculocisternal Perfusion ◽  
Csf Production ◽  
Humoral Regulation

The goal of this study was to examine the role of arginine vasopressin in humoral regulation of choroid plexus function. Production of cerebrospinal fluid (CSF) was measured in anesthetized rabbits with an indicator dilution method, by using ventriculocisternal perfusion of artificial CSF containing blue dextran. Rabbits received either vehicle, vasopressin or vasopressin in the presence of the V1-antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]arginine vasopressin ([d(CH2)5Tyr(Me)]-AVP). Under control conditions, blood flow to the choroid plexus (measured with microspheres) averaged 369 +/- 26 (mean +/- SE) ml.min-1.100 g-1 and CSF production averaged 9.9 +/- 0.9 microliters/min. Intravenous infusion of vasopressin (2 mU.kg-1.min-1 for 90 min) decreased blood flow to the choroid plexus by 50-60% for the entire period of infusion. Vasopressin decreased production of CSF by 35 +/- 8%. Blood flow to the choroid plexus and production of CSF did not change significantly from control values in animals that received vehicle. In the presence of the V1-antagonist (10 micrograms/kg), infusion of vasopressin had no effect on blood flow to the choroid plexus or production of CSF. Thus circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has important effects on formation of CSF, as well as on blood flow to the choroid plexus. These findings are consistent with the hypothesis that effects of vasopressin on both variables are mediated through vasopressin (V1)-receptors.

Opinion of the Pathogenesis of the Mumps Meningites

2020 ◽  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Choroid Plexus ◽  
Present Article ◽  
Clinical Data ◽  
Fluid Secretion ◽  
Mumps Virus ◽  
Direct Involvement ◽  
Glymphatic System ◽  
Cerebrospinal Fluid Secretion

It is generally accepted that meningeal reactions in patients with mumps are due to the direct involvement of the meninges by the mumps virus. With the development of mumps vaccines, this view was extended to vaccinated people, who are considered serious post-vaccine meningitis. In present article, the author states that these reactions are not due to inflammation of the meninges, but to the choroid plexus caused by virulent and vaccine strains. Inflammation leads to an increase in cerebrospinal fluid secretion, which increases intracranial pressure and is manifested by meningeal symptoms. In the presence of this evidence, the author considers that meningeal reactions are not meningitis, but meningisms, based on clinical data, experiments on monkeys and the glymphatic system.

A design of brain port with a built-in bi-directional check valve improves the ventriculostomy

2019 ◽  
Vol 43 (5) ◽  
pp. 348-353
Author(s):  
Taishin Chung ◽  
Ki-Cheol Yoon ◽  
Kwang Gi Kim ◽  
Seung Hoon Lee ◽  
Heon Yoo
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Drug Administration ◽  
Check Valve ◽  
The Other ◽  
Cerebrospinal Fluid Drainage ◽  
Additional Surgery ◽  
Threatening Condition ◽  
Life Threatening ◽  
The Brain

The increase of intracranial pressure is a life-threatening condition which requires urgent treatment to prevent the further neurologic problem. A design of the brain port is proposed, in which a bi-directional check valve controls the flow of the cerebrospinal fluid depending on the intracranial pressure in accordance with the other devices. Drug administration and cerebrospinal fluid drainage could be performed easily without any additional surgery other than the transplant of a brain port. The intracranial pressure value at which the cerebrospinal fluid should be drained is adjustable by altering the pressure of the drainage bag. The results of the experiment with the simulated brain system are supporting and verifying the substance of this article.

scholarly journals Autonomic Nerves in the Mammalian Choroid Plexus and Their Influence on the Formation of Cerebrospinal Fluid

1981 ◽  
Vol 1 (3) ◽  
pp. 245-266 ◽  
Author(s):  
Maria Lindvall ◽  
Christer Owman
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Sympathetic Nerves ◽  
Inhibitory Effect ◽  
Cholinergic Innervation ◽  
Autonomic Nerves ◽  
Pronounced Increase ◽  
Csf Production ◽  
Stimulation Of

The choroid plexuses of all ventricles receive a well-developed adrenergic and cholinergic innervation reaching both the secretory epithelium and the vascular smooth muscle cells. Also peptidergic nerves, containing vasoactive intestinal polypeptide, are present but primarily associated only with the vascular bed. A sympathetic inhibitory effect on the plexus epithelium has been indicated in determinations of carbonic anhydrase activity and by studies of various aspects of active transport in isolated plexus tissue. Pharmacological analysis in vitro has shown the choroidal arteries to possess both vasoconstrictory α-adrenergic and vasodilatory β-adrenergic receptors. Electrical stimulation of the sympathetic nerves, which originate in the superior cervical ganglia, induces as much as 30% reduction in the net rate of cerebrospinal fluid (CSF) production, while sympathectomy results in a pronounced increase, about 30% above control, in the CSF formation. There is strong reason to believe that the choroid plexus is under the influence of a considerable sympathetic inhibitory tone under steady-state conditions. From pharmacological and biochemical experiments it is suggested that the sympathomimetic reduction in the rate of CSF formation is the result of a combined β-receptormediated inhibition of the secretion from the plexus epithelium and a reduced blood flow in the choroid plexus tissue resulting from stimulation of the vascular α-receptors. The choroid plexus probably also represents an important inactivation site and gate mechanism for sympathomimetic amines, as evidenced by considerable local activity of catechol- O-methyl transferase and monoamine oxidase, primarily type B. The CSF production rate is also reduced by cholinomimetic agents, suggesting the presence of muscarinic-type cholinergic receptors in the choroid plexus.

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