Ultrastructural Morphology of the Ependyma and Choroid Plexus in the African Giant Rat (Cricetomys gambianus)

2021 ◽  
Vol 65 (1) ◽  
pp. 45-53
Author(s):  
M. A. Olude ◽  
F. E. Olopade ◽  
O. A. Mustapha ◽  
S. T. Bello ◽  
A. O. Ihunwo ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Brain Parenchyma ◽  
Ependymal Cells ◽  
Apical Surface ◽  
Zonula Occludens ◽  
Cricetomys Gambianus ◽  
Functional Components ◽  
Columnar Cells ◽  
The Brain ◽  
African Giant Rat

Abstract Ependymal cells line the interface between the ventricular surfaces and the brain parenchyma. These cells, in addition to the choroid plexus, form the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) and serve important functions in the protection and regulation of brain metabolism. The African giant rat (AGR) has been used as sentinels to detect potential neuropathology arising from ecotoxicological pollutions. This study examined the lateral ventricular lining by using histology, immunohistochemistry and electron microscopy. Marked variations were observed in some regions of the ventricles which showed multi-layering of ependymal cells that differed from the typical single layered ependymal cells at the apical surface, while subependymal structures revealed indistinctive neuropil and glia following histological examinations. The ependymal cells which form the epithelial lining of the ventricles were comprised of cuboidal or low columnar cells, with the plasmalemma of abutting cells forming intercellular bridge appearing links by: tight junctions (zonula occludens), intermediate junctions (zonula adherens), desmosomes (macula adherens) and infrequent gap junctions. The choroid plexus revealed cells of Kolmer with several cilia and microvilli. The possible functional components of the ependyma and choroid plexus morphology of the AGR are discussed and thus provide a baseline for further research on the AGR brain.

Scanning Electron Microscopy of the Choroid Plexus and Ventricular Wall Ependyma in the Rhesus Monkey

1971 ◽  
Vol 29 ◽  
pp. 270-271
Author(s):  
Philip P. McGrath ◽  
Ronald G. Clark ◽  
John B. Ewell ◽  
John M. Wehrung
Keyword(s):  
Electron Microscopy ◽  
Electron Microscope ◽  
Scanning Electron Microscope ◽  
Choroid Plexus ◽  
Ependymal Cell ◽  
Brain Parenchyma ◽  
Ependymal Cells ◽  
Apical Surface ◽  
Lateral Ventricles ◽  
Scanning Electron

The lumen of the lateral ventricles is separated from the brain parenchyma and the circulatory system by a single layer of specialized epithelial cells, the ependyma. This ependyma is divided into choroid plexus ependymal cells, which coat the pia arachnoid invagination in the lateral ventricles, and the wall ependymal cells which separate the lateral ventricle lumen from brain parenchyma. Using transmission electron microscopy, the ultrastructure of these cells has been described with special emphasis on the difference in apical surface membranes. The apical surface of the choroid plexus ependymal cell contains numerous microvilli and an occasional cilia while the wall ependymal cell contains numerous cilia and only a few microvilli. By scanning electron microscope we have demonstrated differences in the apical surface membrane.The specimens were fixed in glutaraldehyde by vascular perfusion or infusion into the ventricles and postfixed in osmium tetroxide. They were rinsed in cacodylate buffer and three changes of distilled water, blotted dry, and freeze dried, using liquid nitrogen. They were coated with gold palladium and examined in a Cambridge Mark II A stereoscan, scanning electron microscope.

Analysis of Changes in Signal Intensity of Choroid Plexus in MRI Using FLAIR-DW-EPI Pulse Sequence

2020 ◽  
Vol 3 (1) ◽  
pp. 9-15
Author(s):  
Jingyu Kim ◽  
◽  
Sang-Jin Im ◽  
Keyword(s):  
Choroid Plexus ◽  
Signal Intensity ◽  
Pulse Sequence ◽  
Signal Strength ◽  
Brain Parenchyma ◽  
Weighted Image ◽  
Diffusion Weighted ◽  
Water Signal ◽  
The Brain ◽  
Functional Problems

In this study, the signal intensity of choroid plexus, which is producing cerebrospinal fluid, is analyzed according to the FLAIR diffusion-weighted imaging technique. In the T2*-DW-EPI diffusion-weighted image, the FLAIR-DW-EPI technique, which suppressed the water signal, was additionally examined for subjects with high choroid plexus signals and compared and analyzed the signal intensity. As a result of the experiment, it was confirmed that the FLAIR-DW-EPI technique showed a signal strength equal to or lower than that of the brain parenchyma, and there was a difference in signal strength between the two techniques. As a result of this study, if the choroidal plexus signal is high in the T2 * -DW-EPI diffusionweighted image, additional examination of the FLAIR-DW-EPI technique is thought to be useful in distinguishing functional problems of the choroid plexus. In conclusion, if the choroidal plexus signal is high on the T2*-DW-EPI diffuse weighted image, it is thought that further examination of the FLAIR-DW-EPI technique will be useful in distinguishing functional problems of the choroidal plexus.

scholarly journals Senescent Accelerated Prone 8 (SAMP8) Mice as A Model of Age Dependent Neuroinflammation

2020 ◽  
Author(s):  
Andrés Fernández ◽  
Elena Quintana ◽  
Patricia Velasco ◽  
Belén de Andrés ◽  
Maria Luisa Gaspar ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Inflammatory Cytokines ◽  
Hippocampal Formation ◽  
Morphological Changes ◽  
Interleukin 1 ◽  
Brain Parenchyma ◽  
Age Related ◽  
Inflammatory Changes ◽  
Samp8 Mice ◽  
The Brain

Abstract Background: Aging and age related diseases are strong risk factors for the development of neurodegenerative diseases. Neuroinflammation (NIF), as the brain's immune response, plays an important role in aged associated degeneration of central nervous system (CNS). The need of animal models that will allow us to understand and modulate this process is required for the scientific community. Methods: We have analyzed aging-phenotypical and inflammatory changes of brain myeloid cells (bMyC) in a senescent accelerated prone aged (SAMP8) mouse model, and compared with their resistant to senescence control (SAMR1). We have performed morphometric methods to evaluate the architecture of cellular prolongations and analyzed Iba1+ clustered cells with aging. To analyse specific constant brain areas we have performed stereology measurements of Iba1+ cells in the hippocampal formation. We have isolated bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch), and analyzed their response to systemic LPS- driven inflammation.Results: Aged 10 month old SAMP8 mice presents many of the hallmarks of aging-dependent neuroinflammation when compared with their senescence resistant control (SAMR1); ie, increase of protein aggregates, presence of Iba1+ clusters, but not increase in the number of Iba1+ cells. We have further observed and increased of main inflammatory mediator IL-1β, and augment of border MHCII+Iba1+ cells. Isolated CD45+ bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch) have been analyzed showing that there is not significant increase of CD45+ from the periphery. Our data support that aged-driven pro-inflammatory cytokine interleukin 1 beta (IL1β) transcription is mainly enhanced in CD45+BP cells. Furthermore, we are showing that LPS-driven systemic inflammation produces inflammatory cytokines mainly in the border bMyC, sensed to a lesser extent by the BP bMyC, and is enhanced in aged SAMP8 compared to control SAMR1.Conclusion: Our data validate the SAMP8 model to study age-associated neuroinflammatory events, but careful controls for age and strain are required. These animals show morphological changes in their bMyC cell repertoires associated to age, corresponding to an increase in the production of main pro inflammatory cytokines such as IL-1β, which predispose the brain to an enhanced inflammatory response after LPS-systemic challenge.

scholarly journals Spontaneous Ectopic Choroid Plexus with Sclerosis in Adult Beagle Dogs

2018 ◽  
Vol 46 (5) ◽  
pp. 608-609
Author(s):  
Ingrid D. Pardo ◽  
Ahmed M. Shoieb ◽  
Robert Garman ◽  
Michael Mirsky ◽  
Rosemary Santos ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Choroid Plexus ◽  
Neural Development ◽  
Clinical Signs ◽  
Ependymal Cells ◽  
Tubular Structures ◽  
Beagle Dogs ◽  
The Brain ◽  
Morphologic Appearance ◽  
Adjacent Brain

Microscopic examination of the brain of adult Beagle dogs from four different general toxicity studies revealed the presence of ectopic choroid plexus tissue in six individual dogs (4 females and 2 males) with ages ranging from 12 to 18 months. In each dog, this finding was characterized by a well-circumscribed mass localized to a region above and along the corpus callosum without any apparent compression of adjacent brain tissue. Each mass was composed of columnar ependymal cells forming tubular structures surrounded by variable amounts of fibrovascular connective tissue and had the appearance of small rests of ependymal cells that had been penetrated by the leptomeninges during neural development. There were no associated clinical signs or macroscopic correlates. Based on morphologic appearance, a diagnosis of spontaneous ectopic choroid plexus with secondary sclerosis was made. To the authors’ knowledge, ectopic choroid plexus has not been reported in Beagle dogs and is rare in humans and horses.

Treatment Model of CNS Lymphoma Using Complement-Dependent Cytotoxicity Induced by Rituximab and Autoserum.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3739-3739
Author(s):  
Yasuyuki Miyake ◽  
Yasushi Okoshi ◽  
Takayuki Machino ◽  
Shigeru Chiba
Keyword(s):  
Lateral Ventricle ◽  
Raji Cell ◽  
Technical Problem ◽  
Brain Parenchyma ◽  
Autologous Serum ◽  
Ependymal Cells ◽  
Treatment Model ◽  
Complement Dependent Cytotoxicity ◽  
The Brain

Abstract Abstract 3739 Poster Board III-675 Background Primary central nervous system lymphoma (PCNSL) is almost exclusively CD20-positive non-Hodgkin lymphoma (NHL). Although rituximab (R) is widely used for CD20-positive NHL, it is not considered to reach brain lesions effectively beyond the blood brain barrier. Intraventricule administration (ivt) of R is reported to be effective in meningeal lymphoma but the effect on lesions in the brain parenchyma seems to be limited. Recently, a case of refractory PCNSL that was successfully treated with ivt of R with autologous serum was reported (Takami A, et al. Cancer Science, 2006). Because the cerebrospinal fluid does not contain complements which exists in the serum, induction of complement-dependent cytotoxicity by ivt of R plus autoserum was speculated. To investigate this effect, we developed an animal treatment model of CNSL. Materials and methods Raji, CD20-positive Burkitt lymphoma cell line, was inoculated into the deep frontal lobe of the brain of 8-week old F344 (nru-/nru-) nude rats, using brain stereotaxic apparatus. At the same time, a cannula was placed into the ipsilateral lateral ventricle. After several days, R or control immunoglobulin (cIg), plus human serum or saline, was administrated into the lateral ventricle. Results The brain was extracted 24 hours after the last administration and frozen section was made. Human CD20-positive Raji cell tumor was also positively stained with FITC-conjugated anti-human IgG antibody when R but not cIg was administrated. Consequently, R in the lateral ventricle was considered to penetrate ependymal cells and brain parenchyma, and bound to lymphoma cells. Next, these rats were treated with ivt of R plus serum (R + Serum), cIg plus serum (cIg + Serum), or R plus saline (R + saline). These were administrated once a day from day 5 to day 9 after inoculation of Raji, and then survival was monitored. When an obvious weakness, such as marked and consecutively loss of activity or weight, was observed, these rats were euthanized and this is defined as dead day. In each case, the brain was extirpated and examined whether lymphoma existed or not. Death without lymphoma or from technical problem was excluded from the analysis. Survival of each group was analyzed by Kaplan-Meier method and log-lank test. R + Serum group had longer survival than cIg + Serum (p = 0.049). Long-term survivors were only seen in R + Serum and this group seemed to be superior to R + saline but statistical difference was not detected (p = 0.083). There were no difference between cIg + Serum and R + saline (p =0.382) and neither group had long-term survivor. Conclusion The possibility of novel treatment of CNSL with ivt of R and autoserum was shown in the rat CNSL model. To confirm this approach, clinical trials are warranted. Disclosures: No relevant conflicts of interest to declare.

The betaine-GABA transporter (BGT1, slc6a12) is predominantly expressed in the liver and at lower levels in the kidneys and at the brain surface

2012 ◽  
Vol 302 (3) ◽  
pp. F316-F328 ◽  
Author(s):  
Y. Zhou ◽  
S. Holmseth ◽  
R. Hua ◽  
A. C. Lehre ◽  
A. M. Olofsson ◽  
...  
Keyword(s):  
Plasma Membranes ◽  
Renal Medulla ◽  
Brain Parenchyma ◽  
Ependymal Cells ◽  
Main Role ◽  
Mrna Levels ◽  
Physiological Importance ◽  
Brain Surface ◽  
Negative Controls ◽  
The Brain

The Na+- and Cl−-dependent GABA-betaine transporter (BGT1) has received attention mostly as a protector against osmolarity changes in the kidney and as a potential controller of the neurotransmitter GABA in the brain. Nevertheless, the cellular distribution of BGT1, and its physiological importance, is not fully understood. Here we have quantified mRNA levels using TaqMan real-time PCR, produced a number of BGT1 antibodies, and used these to study BGT1 distribution in mice. BGT1 (protein and mRNA) is predominantly expressed in the liver (sinusoidal hepatocyte plasma membranes) and not in the endothelium. BGT1 is also present in the renal medulla, where it localizes to the basolateral membranes of collecting ducts (particularly at the papilla tip) and the thick ascending limbs of Henle. There is some BGT1 in the leptomeninges, but brain parenchyma, brain blood vessels, ependymal cells, the renal cortex, and the intestine are virtually BGT1 deficient in 1- to 3-mo-old mice. Labeling specificity was assured by processing tissue from BGT1-deficient littermates in parallel as negative controls. Addition of 2.5% sodium chloride to the drinking water for 48 h induced a two- to threefold upregulation of BGT1, tonicity-responsive enhancer binding protein, and sodium- myo-inositol cotransporter 1 (slc5a3) in the renal medulla, but not in the brain and barely in the liver. BGT1-deficient and wild-type mice appeared to tolerate the salt treatment equally well, possibly because betaine is one of several osmolytes. In conclusion, this study suggests that BGT1 plays its main role in the liver, thereby complementing other betaine-transporting carrier proteins (e.g., slc6a20) that are predominantly expressed in the small intestine or kidney rather than the liver.

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.

scholarly journals Distribution of Suramin, an Antitrypanosomal Drug, across the Blood-Brain and Blood-Cerebrospinal Fluid Interfaces in Wild-Type and P-Glycoprotein Transporter-Deficient Mice

2007 ◽  
Vol 51 (9) ◽  
pp. 3136-3146 ◽  
Author(s):  
Lisa Sanderson ◽  
Adil Khan ◽  
Sarah Thomas
Keyword(s):  
Choroid Plexus ◽  
Brain Perfusion ◽  
Brain Parenchyma ◽  
Sleeping Sickness ◽  
New Drugs ◽  
Wild Type ◽  
P Glycoprotein ◽  
Blood Brain ◽  
Targeted Mutation ◽  
The Brain

ABSTRACT Although 60 million people are exposed to human African trypanosomiasis, drug companies have not been interested in developing new drugs due to the lack of financial reward. No new drugs will be available for several years. A clearer understanding of the distribution of existing drugs into the brains of sleeping sickness patients is needed if we are to use the treatments that are available more safely and effectively. This proposal addresses this issue by using established animal models. Using in situ brain perfusion and isolated incubated choroid plexus techniques, we investigated the distribution of [3H]suramin into the central nervous systems (CNSs) of male BALB/c, FVB (wild-type), and P-glycoprotein-deficient (Mdr1a/Mdr1b-targeted mutation) mice. There was no difference in the [3H]suramin distributions between the three strains of mice. [3H]suramin had a distribution similar to that of the vascular marker, [14C]sucrose, into the regions of the brain parenchyma that have a blood-brain barrier. However, the association of [3H]suramin with the circumventricular organ samples, including the choroid plexus, was higher than that of [14C]sucrose. The association of [3H]suramin with the choroid plexus was also sensitive to phenylarsine oxide, an inhibitor of endocytosis. The distribution of [3H]suramin to the brain was not affected by the presence of other antitrypanosomal drugs or the P-glycoprotein efflux transporter. Overall, the results confirm that [3H]suramin would be unlikely to treat the second or CNS stage of sleeping sickness.

scholarly journals Spike protein multiorgan tropism suppressed by antibodies targeting SARS-CoV-2

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Molly Brady ◽  
Conor McQuaid ◽  
Alexander Solorzano ◽  
Angelique Johnson ◽  
Abigail Combs ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Imaging System ◽  
Brain Parenchyma ◽  
Dynamic Imaging ◽  
Spike Protein ◽  
Tissue Analysis ◽  
Organ Uptake ◽  
Organ Specific ◽  
The Brain

AbstractWhile there is SARS-CoV-2 multiorgan tropism in severely infected COVID-19 patients, it’s unclear if this occurs in healthy young individuals. In addition, for antibodies that target the spike protein (SP), it’s unclear if these reduce SARS-CoV-2/SP multiorgan tropism equally. We used fluorescently labeled SP-NIRF to study viral behavior, using an in vivo dynamic imaging system and ex in vivo tissue analysis, in young mice. We found a SP body-wide biodistribution followed by a slow regional elimination, except for the liver, which showed an accumulation. SP uptake was highest for the lungs, and this was followed by kidney, heart and liver, but, unlike the choroid plexus, it was not detected in the brain parenchyma or CSF. Thus, the brain vascular barriers were effective in restricting the entry of SP into brain parenchyma in young healthy mice. While both anti-ACE2 and anti-SP antibodies suppressed SP biodistribution and organ uptake, anti-SP antibody was more effective. By extension, our data support the efficacy of these antibodies on SARS-CoV-2 multiorgan tropism, which could determine COVID-19 organ-specific outcomes.

scholarly journals GEMC1-MCIDAS transcriptional program regulates multiciliogenesis in the choroid plexus and acts as a barrier to tumorigenesis

2020 ◽  
Author(s):  
Qun Li ◽  
Zhiyuan Han ◽  
Navleen Singh ◽  
Berta Terré ◽  
Ryann M. Fame ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Tumor Cells ◽  
Hedgehog Signaling ◽  
Ependymal Cells ◽  
Sonic Hedgehog Signaling ◽  
Therapeutic Implications ◽  
Multiciliated Cells ◽  
Ependymal Cilia ◽  
Pediatric Brain ◽  
The Brain

AbstractMulticiliated cells (MCCs) in the brain include the ependymal cells and choroid plexus (CP) epithelial cells. The CP secretes cerebrospinal fluid that circulates within the ventricular system, driven by ependymal cilia movement. However, the mechanisms and functional significance of multiciliogenesis in the CP remain unknown. Deregulated oncogenic signals cause CP carcinoma (CPC), a rare but aggressive pediatric brain cancer. Here we show that aberrant NOTCH and Sonic Hedgehog signaling in mice drive tumors that resemble CPC in humans. NOTCH-driven CP tumors were monociliated, whereas disruption of the NOTCH complex restored multiciliation and decreased tumor growth. NOTCH suppressed multiciliation in tumor cells by inhibiting the expression of GEMC1 and MCIDAS, early regulators of multiciliogenesis. Consistently, GEMC1-MCIDAS function is essential for multiciliation in the CP, and is critical for correcting multiciliation defect in tumor cells by a NOTCH inhibitor. Disturbances to the GEMC1 program are commonly observed in human CPCs characterized by solitary cilia. Consistently, CPC driven by deletion of Trp53 and Rb1 in mice exhibits a cilia deficit consequent to loss of Gemc1-Mcidas expression. Taken together, these findings reveal a GEMC1-MCIDAS multiciliation program in the CP critical for inhibiting tumorigenesis, and it may have therapeutic implications for the treatment of CPC.

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