Cerebrospinal fluid may flow out from the brain through the frontal skull base and choroid plexus: a gold colloid and cadaverine injection study in mouse fetus

Author(s):  
Takuya Akai ◽  
Toshihisa Hatta ◽  
Hiromi Sakata-Haga ◽  
Seiji Yamamoto ◽  
Hiroki Otani ◽  
...  
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 ◽  
...  

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.


2019 ◽  
Vol 34 (1) ◽  
pp. 70-73 ◽  
Author(s):  
Karan Jolly ◽  
Okechukwu Okonkwo ◽  
Georgios Tsermoulas ◽  
Shahzada K. Ahmed

Background Endoscopic skull base surgery continues to push boundaries with increased complexity of work and subsequently larger defects requiring repair. Robust repair following endoscopic skull base surgery is essential to reduce significant postoperative complications such as cerebrospinal fluid leak, meningitis, and pneumocephalus. Objective To describe and further validate our novel technique of using a polydioxanone plate wrap used in large anterior skull base resections where brain herniation can be of concern. Method After large resections where there is obvious brain herniation, our PDS (polydioxanone) wrap can be deployed to provide rigid support to the brain. The PDS plate is wrapped in a dural graft material and sutured closed in order to allow deployment by releasing the sutures when in position under the bony ridge of the defect. Conclusion Till date we have successfully used this technique in 3 patients following large skull base resections of olfactory meningiomas, where there was herniation of the brain. Postoperatively, there was no evidence of cerebrospinal fluid leak. We therefore recommend the use of the PDS wrap to prevent brain herniation and provide additional support to the repair.


Author(s):  
Eelco F. M. Wijdicks ◽  
William D. Freeman

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.


2019 ◽  
Vol 14 (9) ◽  
pp. 923-930 ◽  
Author(s):  
Natalia Egorova ◽  
Elie Gottlieb ◽  
Mohamed Salah Khlif ◽  
Neil J Spratt ◽  
Amy Brodtmann

Background Cerebrospinal fluid circulation is crucial for the functioning of the brain. Aging and brain pathologies such as Alzheimer’s disease have been associated with a change in the morphology of the ventricles and the choroid plexus. Despite the evidence from animal models that the cerebrospinal fluid system plays an important role in neuroinflammation and the restoration of the brain after ischemic brain injury, little is known about changes to the choroid plexus after stroke in humans. Aims Our goal was to characterize structural choroid plexus changes poststroke. Methods We used an automatic segmentation tool to estimate the volumes of choroid plexus and lateral ventricles in stroke and control participants at three time points (at baseline, 3 and 12 months) over the first year after stroke. We assessed group differences cross-sectionally at each time point and longitudinally. For stroke participants, we specifically differentiated between ipsi- and contra-lesional volumes. Statistical analyses were conducted for each region separately and included covariates such as age, sex, total intracranial volume, and years of education. Results We observed significantly larger choroid plexus volumes in stroke participants compared to controls in both cross-sectional and longitudinal analyses. Choroid plexus volumes did not exhibit any change over the first year after stroke, with no difference between ipsi- and contra-lesional volumes. This was in contrast to the volume of lateral ventricles that we found to enlarge over time in all participants, with more accelerated expansion in stroke survivors ipsi-lesionally. Conclusions Our results suggest that chronic stages of stroke are characterized by larger choroid plexus volumes, but the enlargement likely takes place prior to or very early after the stroke incident.


2020 ◽  
Author(s):  
Huixin Xu ◽  
Ryann M Fame ◽  
Cameron Sadegh ◽  
Jason Sutin ◽  
Christopher Naranjo ◽  
...  

ABSTRACTCerebrospinal fluid (CSF) provides vital support for the brain. Abnormal CSF accumulation is deleterious for perinatal neurodevelopment, but how CSF leaves the brain during this critical period is unknown. We found in mice a postnatal neurodevelopmental transition phase featuring precipitous CSF K+ clearance, accompanied by water, through the choroid plexus (ChP). The period corresponds to a human fetal stage when canonical CSF clearance pathways have yet to form and congenital hydrocephalus begins to manifest. Unbiased ChP metabolic and ribosomal profiling highlighted this transition phase with increased ATP yield and activated energy-dependent K+ transporters, in particular the Na+-K+-Cl− and water cotransporter NKCC1. ChP-targeted NKCC1 overexpression enhanced K+-driven CSF clearance and enabled more permissive cerebral hydrodynamics. Moreover, ventriculomegaly in an obstructive hydrocephalus model was improved by ChP-targeted NKCC1 overexpression. Collectively, we identified K+-driven CSF clearance through ChP during a transient but critical neurodevelopmental phase, with translational value for pathologic conditions.


2019 ◽  
Author(s):  
Jihye Kim ◽  
Michal Hetman ◽  
Eyas M. Hattab ◽  
Joshua Joiner ◽  
Brian Alejandro ◽  
...  

ABSTRACTZika virus (ZIKV) can infect and cause microcephaly and Zika-associated neurological complications in the developing fetal and adult brains. In terms of pathogenesis, a critical question is how ZIKV overcomes the barriers separating the brain from the circulation and gains access to the central nervous system (CNS). Despite the importance of ZIKV pathogenesis, the route ZIKV utilizes to cross CNS barriers remains unclear.Here we show that in mouse models, ZIKV-infected cells initially appeared in the periventricular regions of the brain, including the choroid plexus and the meninges, prior to infection of the cortex. The appearance of ZIKV in cerebrospinal fluid (CSF) preceded infection of the brain parenchyma. We show that ZIKV infects pericytes in the choroid plexus, and that ZIKV infection of pericytes is dependent on AXL receptor tyrosine kinase. Using an in vitro Transwell system, we highlight the possibility of ZIKV to move from the blood side to CSF side, across the choroid plexus epithelial layers, via a nondestructive pathway (e.g., transcytosis). Finally, we demonstrate that brain infection is significantly attenuated by neutralization of the virus in the CSF, indicating that ZIKV in the CSF at the early stage of infection might be responsible for establishing a lethal infection of the brain. Taken together, our results suggest that ZIKV invades the host brain by exploiting the blood-CSF barrier rather than the blood-brain barrier.AUTHOR SUMMARYZika virus invades the human brains and causes Zika-associated neurological complications; however, the mechanism(s) by which Zika virus accesses the central nerves system remain unclear. Understanding of the cellular and molecular mechanisms will shed light on development of novel therapeutic and prophylactic targets for Zika virus and other neurotropic viruses. Here we use in vivo and in vitro models to understand how Zika virus enters the brain. In mouse models, we found that Zika virus infects pericytes in the choroid plexus at very early stages of infection and neutralization of Zika virus in the cerebrospinal fluid significantly attenuate the brain infection. Further we show evidence that Zika virus can cross the epithelial cell layers in the choroid plexus from the blood side. Our research highlights that ZIKV invades the host brain by exploiting the blood-CSF barrier rather than the blood-brain barrier.


2005 ◽  
Vol 230 (10) ◽  
pp. 771-776 ◽  
Author(s):  
Janelle S. Crossgrove ◽  
G. Jane Li ◽  
Wei Zheng

β-Amyloid (Aβ) concentration in the cerebrospinal fluid (CSF) of the brain may be regulated by the choroid plexus, which forms a barrier between blood and brain CSF. Aβ uptake from CSF was determined as its volume of distribution (VD) into isolated rat choroid plexus tissue. The VD of [125l]Aβ1–40 was corrected by subtraction of the VD of [14C]sucrose, a marker for extracellular space and diffusion. Aβ uptake into choroid plexus was time and temperature dependent. Uptake of [125l]Aβ was saturable. Aβ uptake was not affected by addition of transthyretin or apolipoprotein E3. In studies with primary culture monolayers of choroidal epithelial cells in Transwells, Aβ permeability across cells, corrected by [14C]sucrose, was greater from the CSF-facing membrane than from the blood-facing membrane. Similarly, cellular accumulation of [125l]Aβ was concentrative from both directions and was greater from the CSF-facing membrane, suggesting a bias for efflux. Overall, these results suggest the choroid plexus selectively cleanses Aβ from the CSF by an undetermined mechanism(s), potentially reducing Aβ from normal brains and the brains of Alzheimer's disease patients.


1990 ◽  
Vol 258 (2) ◽  
pp. R338-R345 ◽  
Author(s):  
G. Schreiber ◽  
A. R. Aldred ◽  
A. Jaworowski ◽  
C. Nilsson ◽  
M. G. Achen ◽  
...  

The transport of thyroxine from the bloodstream to the brain and the synthesis and secretion of transthyretin (formerly called prealbumin) were studied in rats and in sheep choroid plexus perfused in vitro. Rat choroid plexus contained 4.4 micrograms and rat liver 0.39 micrograms transthyretin mRNA per gram wet tissue. The specific radioactivity of transthyretin isolated from cerebrospinal fluid of rats 60 min after intravenous injection of [14C]leucine was greater than 50 times that of transthyretin from serum. After adding [14C]leucine to the perfusion medium of an in vitro perfused sheep choroid plexus, highly radioactive transthyretin was isolated from freshly secreted cerebrospinal fluid collected from the exposed choroid plexus surface. Secretion of newly synthesized transthyretin into the perfusion medium could not be demonstrated. After intravenous injection of [125I]-thyroxine into rats, a maximum in the curve of radioactivity in tissue plotted against time after injection was observed first for choroid plexus, thereafter for cerebrospinal fluid, and still later for cortex and striatum. Based on the obtained data, a hypothesis is derived for the mechanism of the transport of thyroid hormones from the bloodstream to the brain involving transthyretin synthesized in choroid plexus and secreted into the cerebrospinal fluid.


Physiology ◽  
2010 ◽  
Vol 25 (4) ◽  
pp. 239-249 ◽  
Author(s):  
Helle H. Damkier ◽  
Peter D. Brown ◽  
Jeppe Praetorius

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.


Sign in / Sign up

Export Citation Format

Share Document