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 Distribution of Glycylsarcosine and Cefadroxil among Cerebrospinal Fluid, Choroid Plexus, and Brain Parenchyma after Intracerebroventricular Injection is Markedly Different between Wild-Type and Pept2 Null Mice

2010 ◽  
Vol 31 (1) ◽  
pp. 250-261 ◽  
Author(s):  
David E Smith ◽  
Yongjun Hu ◽  
Hong Shen ◽  
Tavarekere N Nagaraja ◽  
Joseph D Fenstermacher ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Interstitial Fluid ◽  
Brain Parenchyma ◽  
Wild Type ◽  
Septal Region ◽  
Biodistribution Studies ◽  
Choroid Plexuses ◽  
Clearance Kinetics ◽  
The Brain

The purpose of this study was to define the cerebrospinal fluid (CSF) clearance kinetics, choroid plexus uptake, and parenchymal penetration of PEPT2 substrates in different regions of the brain after intracerebroventricular administration. To accomplish these objectives, we performed biodistribution studies using [14C]glycylsarcosine (GlySar) and [3H]cefadroxil, along with quantitative autoradiography of [14C]GlySar, in wild-type and Pept2 null mice. We found that PEPT2 deletion markedly reduced the uptake of GlySar and cefadroxil in choroid plexuses at 60 mins by 94% and 82% ( P<0.001), respectively, and lowered their CSF clearances by about fourfold. Autoradiography showed that GlySar concentrations in the lateral, third, and fourth ventricle choroid plexuses were higher in wild-type as compared with Pept2 null mice ( P<0.01). Uptake of GlySar by the ependymal–subependymal layer and septal region was higher in wild-type than in null mice, but the half-distance of penetration into parenchyma was significantly less in wild-type mice. The latter is probably because of the clearance of GlySar from interstitial fluid by brain cells expressing PEPT2, which stops further penetration. These studies show that PEPT2 knockout can significantly modify the spatial distribution of GlySar and cefadroxil (and presumably other peptides/mimetics and peptide-like drugs) in brain.

scholarly journals T-Lymphocytes Traffic into the Brain across the Blood-CSF Barrier: Evidence Using a Reconstituted Choroid Plexus Epithelium

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150945 ◽  
Author(s):  
Nathalie Strazielle ◽  
Rita Creidy ◽  
Christophe Malcus ◽  
José Boucraut ◽  
Jean-François Ghersi-Egea
Keyword(s):  
T Lymphocytes ◽  
Choroid Plexus ◽  
Choroid Plexus Epithelium ◽  
The Brain

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

scholarly journals High Blood Pressure Effects on the Blood to Cerebrospinal Fluid Barrier and Cerebrospinal Fluid Protein Composition: A Two-Dimensional Electrophoresis Study in Spontaneously Hypertensive Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Ibrahim González-Marrero ◽  
Leandro Castañeyra-Ruiz ◽  
Juan M. González-Toledo ◽  
Agustín Castañeyra-Ruiz ◽  
Hector de Paz-Carmona ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Protein Composition ◽  
Pressure Effects ◽  
Apolipoprotein A1 ◽  
Spontaneously Hypertensive ◽  
Barrier Disruption ◽  
Cerebrospinal Fluid Proteins ◽  
The Brain ◽  
Cerebrospinal Fluid Protein

The aim of the present work is to analyze the cerebrospinal fluid proteomic profile, trying to find possible biomarkers of the effects of hypertension of the blood to CSF barrier disruption in the brain and their participation in the cholesterol andβ-amyloid metabolism and inflammatory processes. Cerebrospinal fluid (CSF) is a system linked to the brain and its composition can be altered not only by encephalic disorder, but also by systemic diseases such as arterial hypertension, which produces alterations in the choroid plexus and cerebrospinal fluid protein composition. 2D gel electrophoresis in cerebrospinal fluid extracted from the cistern magna before sacrifice of hypertensive and control rats was performed. The results showed different proteomic profiles between SHR and WKY, thatα-1-antitrypsin, apolipoprotein A1, albumin, immunoglobulin G, vitamin D binding protein, haptoglobin andα-1-macroglobulin were found to be up-regulated in SHR, and apolipoprotein E, transthyretin,α-2-HS-glycoprotein, transferrin,α-1β-glycoprotein, kininogen and carbonic anhidrase II were down-regulated in SHR. The conclusion made here is that hypertension in SHR produces important variations in cerebrospinal fluid proteins that could be due to a choroid plexus dysfunction and this fact supports the close connection between hypertension and blood to cerebrospinal fluid barrier disruption.

scholarly journals Targetable Pathways for Alleviating Mitochondrial Dysfunction in Neurodegeneration of Metabolic and Non-Metabolic Diseases

2021 ◽  
Vol 22 (21) ◽  
pp. 11444
Author(s):  
Lauren Elizabeth Millichap ◽  
Elisabetta Damiani ◽  
Luca Tiano ◽  
Iain P. Hargreaves
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Metabolic Diseases ◽  
Molecular Pathways ◽  
Metabolic Demand ◽  
Neuronal Function ◽  
Attractive Therapeutic Target ◽  
Nervous System Function ◽  
Key Events ◽  
The Brain

Many neurodegenerative and inherited metabolic diseases frequently compromise nervous system function, and mitochondrial dysfunction and oxidative stress have been implicated as key events leading to neurodegeneration. Mitochondria are essential for neuronal function; however, these organelles are major sources of endogenous reactive oxygen species and are vulnerable targets for oxidative stress-induced damage. The brain is very susceptible to oxidative damage due to its high metabolic demand and low antioxidant defence systems, therefore minimal imbalances in the redox state can result in an oxidative environment that favours tissue damage and activates neuroinflammatory processes. Mitochondrial-associated molecular pathways are often compromised in the pathophysiology of neurodegeneration, including the parkin/PINK1, Nrf2, PGC1α, and PPARγ pathways. Impairments to these signalling pathways consequently effect the removal of dysfunctional mitochondria, which has been suggested as contributing to the development of neurodegeneration. Mitochondrial dysfunction prevention has become an attractive therapeutic target, and there are several molecular pathways that can be pharmacologically targeted to remove damaged mitochondria by inducing mitochondrial biogenesis or mitophagy, as well as increasing the antioxidant capacity of the brain, in order to alleviate mitochondrial dysfunction and prevent the development and progression of neurodegeneration in these disorders. Compounds such as natural polyphenolic compounds, bioactive quinones, and Nrf2 activators have been reported in the literature as novel therapeutic candidates capable of targeting defective mitochondrial pathways in order to improve mitochondrial function and reduce the severity of neurodegeneration in these disorders.

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

Intracranial Pressure

2019 ◽  
pp. 69-73
Author(s):  
Eelco F. M. Wijdicks ◽  
William D. Freeman
Keyword(s):  
Cerebrospinal Fluid ◽  
Smooth Muscle ◽  
Choroid Plexus ◽  
Blood Cells ◽  
White Blood Cells ◽  
Ependymal Cells ◽  
Cerebral Aqueduct ◽  
Epithelial Surface ◽  
The Brain ◽  
Route Of Delivery

Cerebrospinal fluid (CSF) fills the subarachnoid space, spinal canal, and ventricles of the brain. CSF is enclosed within the brain by the pial layer, ependymal cells lining the ventricles, and the epithelial surface of the choroid plexus, where it is largely produced. Choroid plexus is present throughout the ventricular system with the exception of the frontal and occipital horns of the lateral ventricle and the cerebral aqueduct. The vascular smooth muscle and the epithelium of the choroid plexus receive both sympathetic and parasympathetic input. In an adult, CSF is normally acellular. A normal spinal sample may contain up to 5 white blood cells (WBCs) or red blood cells (RBCs). CSF allows for a route of delivery and removal of nutrients, hormones, and transmitters for the brain.

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