Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus

2017 ◽  
Vol 23 (8) ◽  
pp. 997-1003 ◽  
Author(s):  
Jason K Karimy ◽  
Jinwei Zhang ◽  
David B Kurland ◽  
Brianna Carusillo Theriault ◽  
Daniel Duran ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Choroid Plexus Epithelium ◽  
Posthemorrhagic Hydrocephalus

Identification and properties of a novel variant of NBC4 (Na+/HCO3− co-transporter 4) that is predominantly expressed in the choroid plexus

2013 ◽  
Vol 450 (1) ◽  
pp. 179-187 ◽  
Author(s):  
Hidekazu Fukuda ◽  
Taku Hirata ◽  
Nobuhiro Nakamura ◽  
Akira Kato ◽  
Katsumasa Kawahara ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Epithelial Cells ◽  
Choroid Plexus ◽  
Apical Membrane ◽  
Recent Observation ◽  
Choroid Plexus Epithelium ◽  
Major Pathway ◽  
Apical Side ◽  
Major Player ◽  
Novel Variant

Secretion of HCO3− at the apical side of the epithelial cells of the choroid plexus is an essential step in the formation of cerebrospinal fluid. Anion conductance with a high degree of HCO3− permeability has been observed and suggested to be the major pathway for HCO3− transport across the apical membrane. Recently, it was found that NBC (Na+/HCO3− co-transporter) 4, an electrogenic member of the NBC family, was expressed in the choroid plexus. We found that a novel variant of the NBC4 [NBC4g/Slc4a5 (solute carrier family 4, sodium bicarbonate co-transporter, member 5)] is almost exclusively expressed in the apical membrane of rat choroid plexus epithelium at exceptionally high levels. RNA interference-mediated knockdown allowed the functional demonstration that NBC4g is the major player in the HCO3− transport across the apical membrane of the choroid plexus epithelium. When combined with a recent observation that in choroid plexus epithelial cells electrogenic NBC operates with a stoichiometry of 3:1, the results of the present study suggest that NBC4g mediates the efflux of HCO3− and contributes to cerebrospinal fluid production.

Active transport of chloride by lateral ventricle choroid plexus of the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F470-F477 ◽  
Author(s):  
Q. R. Smith ◽  
C. E. Johanson
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Active Transport ◽  
Lateral Ventricle ◽  
Bath Temperature ◽  
Methyl Sulfate ◽  
Choroid Plexus Epithelium ◽  
Adult Rat ◽  
Cation Substitutions ◽  
K Transport

The nature of Cl transport and its relation to Na and K transport were analyzed in adult rat lateral ventricle choroid plexus incubated in cerebrospinal fluid (CSF) medium at 37 degrees C and PCO2 = 30 mmHg. In synthetic CSF (extracellular Cl [( Cl]o) = 130 mM), the intracellular Cl [( Cl]i) was three times that estimated for passive distribution. Choroid plexus [Cl]i was not determined by Donnan distribution because [Cl]i remained constant at approximately 50 mM while the [K]i/[K]o ratio was varied 10-fold by drugs and cation substitutions. A [Cl]i/[Cl]o ratio of approximately 0.38 was found when [Cl]o was varied from 15 to 130 mM by isosmotic replacement of Cl with methyl sulfate or isethionate. However, the [Cl]i/[Cl]o ratio increased to greater than 1.0 when [Cl]o was lowered below 5 mM. Reduction in bath temperature to 15 degrees C (CSF PCO2 = 50 mmHg) increased both [Cl]i/[Cl]o and [HCO3]i/[HCO3]o to approximately 0.6. SITS, an inhibitor of Cl-HCO3 transport, reduced [Cl]i by 18 mM, decreasing the [Cl]i/[Cl]o ratio close to the equilibrium value. In contrast, neither furosemide (10(-3) M) nor low CSF [Na]o (3 mM) reduced Cl accumulation. It is concluded that uphill movement of Cl into choroid plexus epithelium occurs primarily by Cl-HCO3 antiport and not by Na-Cl symport.

scholarly journals Epithelial Pathways in Choroid Plexus Electrolyte Transport

Physiology ◽  
2010 ◽  
Vol 25 (4) ◽  
pp. 239-249 ◽  
Author(s):  
Helle H. Damkier ◽  
Peter D. Brown ◽  
Jeppe Praetorius
Keyword(s):  
Cerebrospinal Fluid ◽  
Chemical Composition ◽  
Choroid Plexus ◽  
Interstitial Fluid ◽  
Electrolyte Transport ◽  
Molecular Pathways ◽  
Choroid Plexus Epithelium ◽  
Neuronal Function ◽  
The Brain

A stable intraventricular milieu is crucial for maintaining normal neuronal function. The choroid plexus epithelium produces the cerebrospinal fluid and in doing so influences the chemical composition of the interstitial fluid of the brain. Here, we review the molecular pathways involved in transport of the electrolytes Na+, K+, Cl−, and HCO3− across the choroid plexus epithelium.

A SCL4A10 gene product maps selectively to the basolateral plasma membrane of choroid plexus epithelial cells

2004 ◽  
Vol 286 (3) ◽  
pp. C601-C610 ◽  
Author(s):  
J. Praetorius ◽  
L. N. Nejsum ◽  
S. Nielsen
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Membrane ◽  
Choroid Plexus ◽  
Gene Product ◽  
Pcr Analysis ◽  
Membrane Domain ◽  
Choroid Plexus Epithelium ◽  
Basolateral Plasma Membrane ◽  
Plasma Membrane Domain ◽  
The Brain

The choroid plexus epithelium of the brain ventricular system produces the majority of the cerebrospinal fluid and thereby defines the ionic composition of the interstitial fluid in the brain. The transepithelial movement of Na+ and water in the choroid plexus depend on a yet-unidentified basolateral stilbene-sensitive [Formula: see text]-[Formula: see text] uptake protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed the expression in the choroid plexus of SLC4A10 mRNA, which encodes a stilbene-sensitive [Formula: see text]-[Formula: see text] transporter. Anti-COOH-terminal antibodies were developed to determine the specific expression and localization of this [Formula: see text]-[Formula: see text] transport protein. Immunoblotting demonstrated antibody binding to a 180-kDa protein band from mouse and rat brain preparations enriched with choroid plexus. The immunoreactive band migrated as a 140-kDa protein after N-deglycosylation, consistent with the predicted molecular size of the SLC4A10 gene product. Bright-field immunohistochemistry and immunoelectron microscopy demonstrated strong labeling confined to the basolateral plasma membrane domain of the choroid plexus epithelium. Furthermore, the stilbene-insensitive [Formula: see text]-[Formula: see text] cotransporter, NBCn1, was also localized to the basolateral plasma membrane domain of the choroid plexus epithelium. Hence, we propose that the SLC4A10 gene product and NBCn1 both function as basolateral [Formula: see text] entry pathways and that the SLC4A10 gene product may be responsible for the stilbene-sensitive [Formula: see text]-[Formula: see text] uptake that is essential for cerebrospinal fluid production.

scholarly journals Transport across the choroid plexus epithelium

2017 ◽  
Vol 312 (6) ◽  
pp. C673-C686 ◽  
Author(s):  
Jeppe Praetorius ◽  
Helle Hasager Damkier
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Choroid Plexus ◽  
System Development ◽  
Nervous System Development ◽  
Ionic Balance ◽  
Choroid Plexus Epithelium ◽  
The Central Nervous System ◽  
The Brain

The choroid plexus epithelium is a secretory epithelium par excellence. However, this is perhaps not the most prominent reason for the massive interest in this modest-sized tissue residing inside the brain ventricles. Most likely, the dominant reason for extensive studies of the choroid plexus is the identification of this epithelium as the source of the majority of intraventricular cerebrospinal fluid. This finding has direct relevance for studies of diseases and conditions with deranged central fluid volume or ionic balance. While the concept is supported by the vast majority of the literature, the implication of the choroid plexus in secretion of the cerebrospinal fluid was recently challenged once again. Three newer and promising areas of current choroid plexus-related investigations are as follows: 1) the choroid plexus epithelium as the source of mediators necessary for central nervous system development, 2) the choroid plexus as a route for microorganisms and immune cells into the central nervous system, and 3) the choroid plexus as a potential route for drug delivery into the central nervous system, bypassing the blood-brain barrier. Thus, the purpose of this review is to highlight current active areas of research in the choroid plexus physiology and a few matters of continuous controversy.

scholarly journals NLRP3 inflammasome-mediated cerebrospinal fluid hypersecretion in choroid plexus contributes to hydrocephalus after hemorrhage

2020 ◽  
Author(s):  
Zhaoqi Zhang ◽  
Qiang Tan ◽  
Peiwen Guo ◽  
Zhengcai Jia ◽  
Xin Liu ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Nlrp3 Inflammasome ◽  
Therapeutic Strategy ◽  
Autologous Blood ◽  
Major Protein ◽  
Choroid Plexus Epithelium ◽  
Barrier Integrity ◽  
The Relationship

Abstract BackgroundHydrocephalus is a severe complication of intracerebral hemorrhage with ventricular extension (ICH-IVH). The choroid plexus epithelium plays an important role in cerebrospinal fluid (CSF) secretion and constitutes blood-CSF barrier adjusting brain–immune system interface. NLRP3 inflammasome is a key component of the innate system which promotes neuroinflammation. However, the role of NLRP3 inflammasome in the pathogenesis of hydrocephalus after hemorrhage has not been investigated.MethodsHydrocephalus after ICH-IVH rat model was accomplished by autologous blood infusion. Then, we investigated the relationship between NLRP3 inflammasome and CSF hypersecretion in choroid plexus.ResultsThe NLRP3 inflammasome activated and CSF hypersecretion in choroid plexus epithelium were found after ICH-IVH. NLRP3 inhibition with MCC950 decreased CSF secretion, ventricles dilation and attenuated neurofunction deficits after ICH-IVH. In addition, MCC950 decreased NKCC1 phosphorylation which was the major protein adjusting CSF secretion and improved blood-CSF barrier integrity after ICH-IVH.ConclusionsThis study demonstrates that NLRP3 inflammasome mediated CSF hypersecretion by influencing NKCC1 phosphorylation in choroid plexus epithelium plays an important role in the pathogenesis of hydrocephalus after hemorrhage and provides a new therapeutic strategy.

scholarly journals Multidrug resistance protein 1 protects the choroid plexus epithelium and contributes to the blood-cerebrospinal fluid barrier

2000 ◽  
Vol 105 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Jan Wijnholds ◽  
Elizabeth C.M. de Lange ◽  
George L. Scheffer ◽  
Dirk-Jan van den Berg ◽  
Carla A.A.M. Mol ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Multidrug Resistance ◽  
Choroid Plexus ◽  
Multidrug Resistance Protein ◽  
Choroid Plexus Epithelium ◽  
Multidrug Resistance Protein 1 ◽  
Resistance Protein

Organization of tight junctions in the choroid plexus epithelium

1978 ◽  
Vol 36 (2) ◽  
pp. 336-337
Author(s):  
B. Van Deurs ◽  
J. K. Koehler
Keyword(s):  
Choroid Plexus ◽  
Present Report ◽  
Freeze Fracture ◽  
Barrier Properties ◽  
Cell Junctions ◽  
Structural Basis ◽  
Apical Surface ◽  
Choroid Plexus Epithelium ◽  
Solid Nitrogen ◽  
Special Composition

The choroid plexus epithelium constitutes a blood-cerebrospinal fluid (CSF) barrier, and is involved in regulation of the special composition of the CSF. The epithelium is provided with an ouabain-sensitive Na/K-pump located at the apical surface, actively pumping ions into the CSF. The choroid plexus epithelium has been described as “leaky” with a low transepithelial resistance, and a passive transepithelial flux following a paracellular route (intercellular spaces and cell junctions) also takes place. The present report describes the structural basis for these “barrier” properties of the choroid plexus epithelium as revealed by freeze fracture.Choroid plexus from the lateral, third and fourth ventricles of rats were used. The tissue was fixed in glutaraldehyde and stored in 30% glycerol. Freezing was performed either in liquid nitrogen-cooled Freon 22, or directly in a mixture of liquid and solid nitrogen prepared in a special vacuum chamber. The latter method was always used, and considered necessary, when preparations of complementary (double) replicas were made.

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