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At least 19 recordsLinked to original sources
PubMed1986

[Comparative scanning and transmission electron microscopy studies of the ependyma of the central canal in the spinal cord of primates. I. Electron optical image of the ependyma in the central canal of the spinal cord of the callithrix monkey (Callithrix jacchus, Linné 1758)].

The ependyma lining the central canal of the spinal cord of adult males and females monkey, Callithrix jacchus, was examined by scanning and transmission electron microscopy. The cross section of the lumen of the central canal are round, oval, or triangular. Light and dark ependymal cells, depending on the density of the cytoplasm, were found. The light ependymal cells are fewer than the dark cells. The ependyma cytoplasm contained numerous mitochondria, filamentous structures, one or more well-developed Golgi-complexes, vesicles of the smooth endoplasmic reticulum, ribosomes, lysosomes, multivesicular bodies, profiles of the rough endoplasmic reticulum, large osmophilic bodies, and microtubules. The nuclei of the ependyma cells usually have a simple, regular round or oval shape. They occupy a relatively large portion of the cell volume and lie in the central or mediobasal position. Some of the nuclei show deep invaginations into the karyoplasm. Most of the mitochondria occupy mainly the supranuclear portion of the apical cytoplasm. There are of the crista-typ. Ribosomes occur free in the cytoplasm, but some attached to the profiles of the rough endoplasmic reticulum or being arranged as polysomes. The filamentous structures are generally prominent cytoplasmic components and are distributed at the apical, lateral, or basal region of the ependymocytes. They are grouped into bundles and arranged in parallel arrays. Some of these bundles reach the plasmamembrane at the free lumina of the central canal, others take contact to the filamentous structures of the zonulae adherentes of the junctional complex below the free surface. The granular endoplasmic reticulum shows specializations. There profiles surrounding granular substances and widely distributed granulations in connection with the nuclear envelope. The functional significance of the deposition of these granulations is still unknown. The luminal surface of the ependymocytes bears many microvilli and cilia. The cilia are regularly arranged in cranio-caudal direction. Each cilium has the typical (9 + 2)-subfibres. The intercellular space at the surface of the ependymal layer shows a single zonula adherens or zonulae adherentes in the row. Tight junctions and gap junctions were not found in the material examined. Cell processes of liquor contacting neurons between adjacent ependyma cells, protruding into the lumen of the central canal, could be observed. The termination of these neurons contains accumulations of mitochondria in the central part, large amounts of vesicles, and small dense bodies. They have short microvilli and some stereocilia at the free surface.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

A stereological study of the ependyma of the mouse spinal cord. With a comparative note on the choroid plexus ependyma.

Applying different stereological techniques, the total ependymal volume in the spinal cord of mice was estimated to be 83 x 10(6) microns cubed, the number of cells to be 163,000 and the mean ependymal cell volume to be 510 microns cubed. Compared to choroid plexus cells in the third ventricle, the ependymal cells in the spinal cord contained a smaller mitochondrial volume (9.8% versus 4.6% of cell volume) and less rough endoplasmic reticulum (2.1% versus 0.4%). These findings indicate that the metabolic activity of the ependyma in the spinal cord is lower than that in the choroid plexus. Compared to liver and exocrine pancreatic cells, ependymal cells in both locations must be considered to have a rather low metabolic activity.

Animals↗
PubMed1994

Hyperechoic thickened ependyma: sonographic demonstration and significance in neonates.

In the neonate, hyperechoic thickening of the ependyma is believed to be related to ventriculitis. Yet, in our experience, this sign is much more often observed in association with subacute intraventricular hemorrhage (IVH), without infection. Sixty premature neonates were prospectively studied. The observations of transfontanellar sonograms (intracranial hemorrhage, ependymal echogenicity, and ventriculomegaly) were correlated with the results of MRI, lumbar punctures and clinical work-up. Intracranial hemorrhage was detected in 28 patients, and hyperechoic thickening of the ependyma was observed in 21 of them, all of whom had IVH. In 9 of these 21 patients IVH was diagnosed retrospectively thanks to the visualization of the hyperechoic ependyma. In all but one, this sign persisted for at least 2 months after disappearance of other signs of IVH. MRI demonstrated the presence of hemosiderin and ferritin in ependymal or subependymal location only in patients with hyperechoic ependyma. One of our patients had in utero diagnosis of IVH owing to the visualization of the same hyperechoic aspect of the ependyma. Nine of the neonates with hyperechoic ependyma developed ventriculomegaly, and three underwent surgery. Hyperechoic thickening of the ependyma in prematures often results from a subacute IVH. It is related to hemoglobin catabolites which can be detected by MRI. It does not require immediate potentially harmful diagnostic punctures. The presence of this hyperechoic rim allows a retrospective diagnosis of IVH and indicates a clinical and sonographic follow-up in newborns at risk for secondary hydrocephalus.

Cerebral Hemorrhage↗
PubMed1998

Histochemistry and immunocytochemistry of the developing ependyma and choroid plexus.

The adult human ependyma expresses no intermediate filament proteins or secretory proteins; the fetal ependyma shows strong immunocytochemical (ICC) expression of vimentin, glial fibrillary acidic protein (GFAP), cytokeratins (CKs) of high molecular weight, glycoproteins, and S-100beta protein. Each has a precise and specific spatial distribution within the developing ependyma and a predictable time of appearance and regression in each region of the ventricular system. Several are coexpressed, but some appear earlier or persist longer than others. Secretory proteins of ependymal cells are important in several developmental processes such as the guidance of axonal growth cones. GFAP is not expressed in the floor plate ependyma at any stage of development, unlike vimentin and CK. The choroid plexus epithelium is a specialized ependyma, with an ICC profile that differs from the surface ependyma: vimentin, CK, and S-100beta protein continue to be expressed throughout fetal and adult life, but GFAP is not expressed. Certain cerebral malformations are associated with specific ICC abnormalities: ependymal S-100beta protein continues to be immunoreactive in disorders of neuroblast migration; ependymal vimentin is focally upregulated in Chiari malformations and congenital aqueductal stenosis. Other mammalian and nonmammalian species have characteristic profiles of ependymal immunoreactivity to the same proteins expressed in humans but exhibit interspecific differences.

Animals↗
PubMed2000

Ependymal explants from the lateral ventricle of the adult bovine brain: a model system for morphological and functional studies of the ependyma.

By gently scraping off the surface of the lateral ventricles of adult bovine brains, we obtained sheets containing the ependymal layer and some attached sub-ependymal cells. Explants were cultured in serum-free medium or in two media enriched with 20% fetal calf serum or 20% adult bovine cerebrospinal fluid, and processed for different time intervals from 4 h to 60 days. For characterization of the ependymal cells we used antisera against S-100 protein, vimentin and glial fibrillary acidic protein (GFAP). For comparison, the ependyma of adult bovines and of fetuses from days 60 to 120 post coitum was studied in situ. The adult ependyma consisted of a ciliated, cuboid cell monolayer with short basal processes; it displayed S-100 immunoreactivity but only scarce deposits of vimentin and no GFAP. The fetal ependyma had the appearance of a pseudostratified epithelium with elongated nuclei and basal processes containing S-100 and vimentin from day 80 post coitum and GFAP from day 100 post coitum. In explants, no differences were seen between the three culture media; the ependyma became pseudostratified, developed basal processes and showed increasing amounts of S-100 and vimentin first, and subsequently also GFAP. These changes were concomitant with the onset of mitotic activity in the subependymal layer leading to the production of numerous cells. The morphological and immunocytochemical features of ependymal cells in cultured explants resembled those of fetal ependyma. Our results indicate that the culture of ependymal explants from adult bovine lateral ventricles is an useful model system for morphological and functional studies of the ependyma and for the analysis of cell proliferation in the subependymal layer.

Age Factors↗
PubMed1985

Ependyma: normal and pathological. A review of the literature.

A review of the available literature reveals that proliferation of ependyma occurs during embryological and early postnatal periods of development. Turnover, however, declines significantly during postnatal life and only low levels of residual activity persist into adulthood under normal conditions. In some regions of the ventricle, however, morphological and histochemical differentiation of ependyma is not attained for some considerable time postnatally. Recent immunocytochemical studies using GFAP indicate that only tanycytes may acquire antigenicity during development and that they may share a common phylogeny and/or function with astrocytes. Under pathological conditions, the bulk of available evidence suggests that inherent differences may exist in the proliferative capacity of ependyma in different regions of the neuraxis. Although the response of ependyma to various pathological conditions is equivocal, proliferation has been often observed in response to spinal cord injury. Indeed, ependyma is believed to play a significant role in the initiation and maintenance of the regenerative processes in the spinal cord of inframammalian vertebrates. In hydrocephalus there appears to be a remarkable similarity in cytopathological changes regardless of the mode of induction. The sequence, severity and extensiveness of damage appear to correlate with the degree of ventricular dilatation. The most commonly observed changes are (1) stretching and flattening of ependyma, most pronounced over white matter, (2) characteristic ependymal cell surface changes associated with ventricular distension, (3) increased extracellular space and periventricular edema and (4) demyelination and subependymal gliosis. Although ependymal cell proliferation has been reported as part of the overall tissue response to chronic hydrocephalus and to the pathology of ventricular shunt occlusion, the evidence is not entirely convincing and there is clearly a need for further research on the subject.

Animals↗
PubMedDate not supplied

Role of human fetal ependyma.

Fetal ependyma is an active secretory structure for the programming of developmental events, including the arrest of neuronogenesis, the guidance of axonal growth cones, motor neuron differentiation, and probably also the maintenance and transformation of radial glial cells that guide migratory neuroblasts. The floor plate, induced by the notochord, is the first part of the neuroepithelium to differentiate. It establishes polarity and growth gradients of the neural tube and has immunohistochemical features that differ from all other regions of the ependyma. The dorsal and ventral median septa, formed by floor and roof plate ependymal processes, prevent aberrant decussations of developing long tracts, but permit the passage of commissural axons. Fetal ependyma synthesizes several intermediate filament proteins absent from mature ependymal cells, although some are also expressed in undifferentiated neuroepithelial cells. Fetal ependyma also produces diffusible molecules, such as neural cell adhesion molecule, proteoglycans, nerve growth factor, and S-100 protein, all in specific temporal and spatial distributions. Maturation of the ependyma is not complete until the postnatal period. An abnormal fetal ependyma may play a primary role in the pathogenesis of some cerebral malformations, such as lissencephaly/pachygyria and holoprosencephaly.

Brain↗
PubMed1999

Cell proliferation and nestin expression in the ependyma of the adult rat spinal cord after injury.

A population of precursor cells is known to exist in the subependyma of the lateral ventricles in adult rodents. However, the source of the precursor cells in the adult mammalian spinal cord has not been identified in vivo, although the adult spinal cord was recently reported to contain neural stem cells in vitro. In this study we found active cell proliferation and nestin expression in the adult ependyma of the central canal after spinal cord injury. The normal ependyma showed limited proliferative activity indicated by a low Ki-67 labeling index (1.5% at T1 level) and no immunoreactivity to nestin, a marker for neural precursor cells. In contrast, the spinal cord injured by clip compression demonstrated a dramatic increase in ependymal proliferation indicated by a high Ki-67 labeling index (maximum of 26% at 3 days [d] after injury) and concomitant strong nestin expression in the ependyma. These responses were downregulated by 7 d after injury. The increased cell proliferation in the ependyma was observed only at sites immediately adjacent to the lesion. After injury, nestin positive, GFAP negative cell populations were found in areas surrounding the ependymal layer, which suggests migration of the ependymal cells. These results indicate the precursor cell qualities of the adult ependyma after injury. Thus, we propose the ependyma of the central canal, which is normally latent but activates locally and temporally in response to spinal cord injury, as the in vivo source for precursor cells in the adult mammalian spinal cord.

Animals↗
PubMed1995

Adhesion and fusion of ependyma in rat brain.

Changes of the ependyma of the rat brain from 2 days after birth to 1 year were studied. In neonatal rats, the ependyma of the lateral ventricle extended medially to cover the hippocampus. The ependyma above the hippocampus disappeared with age in two ways: (1) a zipper-like withdrawal of the medial portion of the ventricle towards the lateral direction, and (2) adhesion and fusion of the ependyma in the lateral region. The zipper-like closure and fusion, which resulted in disappearance of the ependyma, took place in almost all rats within 2 or 3 weeks after birth. Initially, ependymal cells retained their cell polarity with regular organization at adhesion sites as a two-cell-layer seam. Subsequently, their polarity became disorganized in the fusion areas with convergence of the two-cell-layer seam into a one-cell-layer seam, followed by disruption. The ciliary bundle of individual ependymal cells became randomly oriented, sometimes in two or more directions. At the sites where fusion had occurred, fragmentary ependymal seams remained detectable (more than 50%) among the neuropil even in adults. These ectopic seams often contained cystic ependymal cells. In the third ventricle, adhesion was observed but fusion was not. The results indicate that adhesion and fusion of the ependyma occur in select areas during brain development, during which ependymal cells lose their cell polarity.

Animals↗
PubMed1990

Formation of multiple ependymas in the regenerating optic lobe of larvae of the Egyptian toad, Bufo regularis Reuss.

In the regenerating optic lobe of Bufo regularis larvae, secondary ependymas were formed in both the dorsal part (optic tectum) and ventral region (tegmentum) of the lobe concerned. These secondary ependymas were frequently observed in the rostral and caudal tectal regions after complete excision of the tectum. Most of the multiple ependymal structures were formed by self-organization of groups of undifferentiated cells migrating from the primary ependyma lining the optic tectum. Others split off from the primary ependyma, but remained in contact with it. The observations emphasize the wide range of possibilities of the cells produced by the larval tectal ependyma in response to partial or total excision of the tectum. The results suggest that cells of ependymal origin, in regenerating tectum, are capable of self-organization to complete ependymal tubes in the absence of direct with the primary ependyma.

Animals↗
PubMed1985

[Morphologic picture of the ependyma of the 3d cerebral ventricle in ewes after hormonal stimulation].

The ependyma in the infundibular region of the third cerebral ventricle was studied. Ageline sponges (20 mg per animal) were applied to nine ewes. On the thirteenth day after the removal of sponges, 750 I. U. PMSG was administered intramuscularly to three ewes, 1000 I. U. PMSG to another three, and the remaining three ewes were left without this treatment. Six ewes were the control. After embedding in paraffin, the material obtained from four control sheep and all the test sheep was stained with haematoxylin-eosine, material from another two control animals was impregnated by the method after Golgi-Cox. The ependyma in the infundibular region of anoestric ewes has a single layer and is cubic to cylindrical; it is only in the recessus infundibuli that it forms two to four layers. After the administration of Ageline, or in combination with PMSG, ependyma can be observed to react within the whole infundibular region of the third cerebral ventricle, but the most expressive reaction is recorded in the caudal part of the middle third of infundibulum where a transient type of cells (between ependymal cells and tanycytes) was found in the control animals after impregnation (they have cilia and one to two short and one long processes). After Ageline administration, ependymal cells in the middle third stretch out like in the anoestric period. The administration of 20 mg Ageline and 750 I. U. PMSG gave rise to low digital excrescences, the ependyma is undulated (pseudo-stratified) or contains small deposits of multiplied cells. After the administration of 20 mg Ageline and 1000 I. U. PMSG, the middle third contained, besides subependymal serous infiltrate, also large digital excrescences, probably filled with a serous fluid, and the surface of the subependyma and ependyma is eroded, containing proliferated deposits of ependymal cells of different thickness. Everywhere proliferation occurs, the surface layer of ependymocytes is desquamated into the cerebrospinal fluid. The histological picture described in the present paper probably suggests an increased secretory activity of ependymal cells after the administration of hormonal preparations. It is confirmed by these results that ependyma is involved in the hypothalamo-hypophyseal control of the sexual activity of sheep.

Animals↗
PubMed1997

Central innervation of the rat ependyma and subcommissural organ with special reference to ascending serotoninergic projections from the raphe nuclei.

The subcommissural organ (SCO) and the cerebral ependyma receive serotoninergic innervation, but little is known about their origin in the raphe nuclei. Application of the retrograde tracer cholera toxin subunit B (ChB) in the third ventricle resulted in uptake in ependymal axons and backfilling of perikarya in the dorsomedian part of the dorsal raphe nucleus, immediately under the caudal aqueduct. By using dual staining with antisera against serotonin and ChB, a portion of the retrogradely labeled neurons was observed to co-store serotonin. Phaseolus vulgaris-leucoagglutinin (PHA-L) was injected into different raphe nuclei to fill the neurons in the same areas where the retrogradely labeled neurons were found. PHA-L injection in the midline of the dorsal raphe nucleus gave rise to ascending axonal processes in the mesencephalic central gray, from where they entered the periventricular strata and the third ventricular ependyma. In the cerebral ependyma, large numbers of positive fibers were consistently found in the ventral part of the lateral ventricles and in the dorsal part of the third ventricle. A large number of PHA-L-immunoreactive fibers were observed in the hypendymal layer of the lateral part of the SCO. Terminal fibers near the ependymal cells were also observed. In all cases, the PHA-L injections labeled innervating fibers both within the ependyma and in the SCO, whereas injections into the median raphe nucleus or in other raphe nuclei (i.e., the raphe pallidus and the raphe pontis) labeled fibers neither in the SCO nor in the ependyma. This study shows that a specific group of predominantly serotoninergic neurons innervates both the ependyma and the SCO and is probably involved in cerebrospinal fluid regulation.

Animals↗
PubMed1995

Development of ependyma in neural transplants.

Under in situ conditions, the innermost (juxtaventricular) neuroepithelial layer of the embryonic brain wall develops into ependyma. No development of ependyma was usually observed, however, in transplanted embryonic brain wall. In our telencephalic transplants, however, cysts lined by epithelium resembling ependyma were observed, although only sporadically. We supposed that occasional foldings of the transplanted telencephalic wall enclosed the aforementioned cysts and so induced the formation of ependyma. This hypothesis was supported by the observation that ependyma developed frequently in a model system in which the telencephalic wall was folded artificially prior to transplantation.

Brain Diseases↗
PubMed1996

The supra-ependymal innervation is not responsible for the repression of tight junctions in the rat cerebral ependyma.

Classically, the contiguous epithelial cells show intercellular tight junctions (TJ) positioned as a continuous belt of cell-cell contacts at the boundary of apical and basolateral plasma membranes. Among the epithelia, the "typical" cerebral ependyma is very peculiar due to the absence of TJ, in contrast to the ependyma of the circumventricular organs (e.g. choroid plexus and the subcommissural organ) which shows well differentiated TJ. Since the "typical" ependyma is covered in the rat with a plexus of intraventricular nervous fibres not present at the surface of the circumventricular organs, we hypothesized local repression of TJ by molecules (serotonin, GABA, etc.) released by the supra-ependymal varicosities. Neither the denervation of the "typical" ependyma nor the ex vivo activation of protein kinase C (which increases the transepithelial resistance as it has been reported in other epithelia) produced junctional fibrils as shown by freeze-fracture. As the protein ZO-1 was not detectable in the "typical" ependyma by immunocytochemistry, there is probably repression of the genes responsible for TJ biosynthesis by unidentified endogenous factors.

5,7-Dihydroxytryptamine↗
PubMed1989

Distribution of epithelial membrane antigen in normal and neoplastic human ependyma.

The ependyma and choroid plexus of 23 normal brains and 20 ependymal tumors were examined immunohistochemically for expression of epithelial membrane antigen (EMA) using a specific monoclonal antibody. The ependyma of normal brains showed three patterns of immunoreactivity: membrane immunoreactivity confined to the luminal surface; irregular punctate intracytoplasmic immunoreactivity in the subependymal layer; and spherical and ring-like intracytoplasmic immunoreactivity in the subependymal layer. Of 13 differentiated ependymomas 11 reflected the immunoreactive patterns of normal ependyma. The anaplastic ependymomas and ependymoblastomas had no immunoreactivity. Our results indicate that EMA has a highly selective distribution in the ependyma, and is a marker for differentiated ependymoma.

Adult↗
PubMed1993

Expression of neuropeptide processing enzymes and neurosecretory proteins in ependyma and choroid plexus epithelium.

Recent studies suggest that brain ependyma and choroid plexus produce neuropeptide processing enzymes. To facilitate the understanding of these cells and their ability to produce biologically active peptides, we developed cultures of defined cell type. Ependymal cells were characterized by morphological criteria, and choroid plexus epithelial cell lines were characterized by the presence of the mRNA for IGF-II and transthyretin, a thyroxine binding protein produced in liver and choroid plexus. The ependymal cells and the choroid plexus epithelial cell lines were then examined for the presence of mRNAs for various neuropeptide processing enzymes. Northern blot analysis revealed high levels of furin, carboxypeptidase E, and peptidyl glycine alpha-amidating monooxygenase mRNAs, with levels in ependymal cells comparable to those in brain or pituitary. Carboxypeptidase E activity was detected in medium from cultured ependymal cells; this activity was identified as carboxypeptidase E based on the acidic pH optimum and sensitivity to various inhibitors. The mRNAs for other neuropeptide processing enzymes, such as prohormone convertases 1 and 2, were not detected on Northern blots of RNA from ependyma or choroid plexus epithelium. Since ependyma and choroid plexus epithelium express a subset of processing enzymes, we suggest that these cells have the capacity to produce biologically active peptides. Initial screening by reverse transcriptase-polymerase chain reaction assays has demonstrated the presence of mRNA for the neurosecretory proteins chromogranin B and secretogranin II in both ependyma and choroid plexus epithelium.

Animals↗
PubMed1998

Curly fiber and tangle-like inclusions in the ependyma and choroid plexus--a pathogenetic relationship with the cortical Alzheimer-type changes?

The question of whether thread- and tangle-like inclusions of the choroid plexus (known as Biondi inclusions) are related to the cortical lesions in Alzheimer disease (AD) has been debated for almost a century, yet remains unanswered. Recently beta-amyloid protein was biochemically isolated from the plexus, indicating a possible pathogenetic relationship between the degenerative changes of the cerebral cortex and those of the plexus. The goal of the present study was to analyze whether or not a significant correlation exists between the occurrence of the cortical AD-type changes and those in the ependyma and choroid plexus. In 292 consecutive autopsy cases several cortical areas, the ependyma, and the choroid plexus were analyzed to look for AD-type changes and Biondi inclusions using histochemical staining techniques and immunohistochemistry. A semiquantitative analysis of the density of cortical AD-type changes showed that of the 292 cases, 63 had severe cortical changes, 23 moderate changes, and 142 discrete changes. In 64 cases no plaques or neurofibrillary tangles were found. The number of cases with thread- and tangle-like elements in the plexus and ependyma was more than 96% in the 3 groups with cortical AD-type lesions, but low in the group without AD-type cortical changes (19%). The pathological argyrophilic filaments accumulating in the ependymal layer and plexus had histochemical properties of amyloid and were immunoreactive with antibodies to P component, ubiquitin, fibronectin and Tau protein. They did not react with antibodies to neurofilament proteins. Ultrastructurally, they consisted of densely packed straight and paired helical filaments and closely resembled neurofibrillary tangles and neuropil threads. The highly significant correlation (chi2, p = 0.001; R = 0.85) between the occurrence of AD-type changes in the cortex and those in ependyma and plexus suggests a pathogenetic relationship.

Alzheimer Disease↗