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At least 217 records · Page 12Linked to original sources
PubMed2002

Damage to the choroid plexus, ependyma and subependyma as a consequence of perinatal hypoxia/ischemia.

Cerebral hypoxia/ischemia (H/I) of the premature infant is a major cause of cerebral palsy and mental retardation. An important determinant of the ultimate outcome from this insult is the extent to which the stem cells and progenitors in the brain are affected. Irreversible injury to these cells will impair normal development of the infant's brain and, hence, its function. In the present study, we examine early intervals after H/I to identify which cells in the periventricular region are most vulnerable. At 0 h of recovery from a perinatal H/I insult, the choroid plexus shows extensive necrotic damage. The adjacent ependymal and subependymal cells are also affected. Swelling of the ependymal and medial subependymal cells is observed; however, these cells rarely sustain permanent damage. By contrast, cells in the most lateral aspect of the subventricular zone (SVZ) show more delayed, but extensive apoptotic and hybrid cell deaths. Interestingly, activated macrophages/microglia are observed adjacent to the swollen ependymal cells as well as within the affected subependyma. We conclude that the choroid plexus is an especially vulnerable structure in the immature brain, whereas the ependymal and adjacent subependymal cells are relatively resistant to damage. As the medial aspect of the SVZ contains neural stem cells, we predict that neural stem cells will be especially resistant to perinatal H/I brain damage.

Animals↗
PubMed1975

Histological and histochemical study on the ependyma of Bradypus tridactylus.

Histological and histochemical aspects of the whole encephalic ventricular system of eight specimens of Bradypus tridactylus were studied. After anesthesia and perfusion, the encephalons were obtained by craniotomy. Transverse serial sections of the encephalon, stained according to Azan (Heidenhain's method) or Kluver-Barrera for nerve cells and myelinated nerve fibers; silver impregnation was carried out according to Cajal-De Castro's or Palmgren's methods. The following histochemical reactions were used: PAS (McManus), metachromasia, acid phosphatase (Gomori), Brachet's and Gomori's trichromic reaction (modified by Bargmann for neurosecretion). Histologically, different characteristics of the ependymal cells in different areas were observed, which would be related to functional peculiarities of each area of the encephalic ventricles. The ependymal cells showed discrete apical basophilia due to the presence of RNA which disappears after treatment with crystalline ribonuclease. The PAS reaction indicated the presence of a small quantity of PAS-positive substances in the apical zone of the ependymal cells and the subependymal tissue. These substances disappeared after the salivary amylase test, indicating the presence of glycogen. The acid phosphatase reaction was negative.

Aminosalicylic Acids↗
PubMed1976

Ultrastructural study on topographical variations of the ependyma in Bradypus tridactylus.

An electron-microscopic study of ependymal cells in 24 different areas of the encephalic ventricular system of Bradypus tridactylus was made, with a view to making a comparative analysis, of a topographical kind, of various cell components: cilia, microvilli, plasma membrane, cytoplasmic protrusions, types of cellular junctions, ribosomes, Golgi apparatus, endoplasmic reticulum, microfilaments, microtubules, mitochondria, granules and dense bodies. There were differences in the distribution of all these cytologic elements, according to the topography, being a complement to a similar work done by the same authors with light-microscopy. By means of a morphofunctional analysis they draw the conclusion that even if one can admit the passage of substances by an intracellular route, on the other hand few facts support the idea the intracellular absorption or secretion could be considered as important phenomena in a great number of the ependymal areas studied.

Animals↗
PubMed1982

Scanning and transmission electron microscopy of the ependyma of the fourth ventricle in the monkey brain.

The ependymal structure of the fourth ventricle floor of adult rhesus monkeys was investigated using both scanning and transmission electron microscopy. Each half of the floor exhibited dense ciliation which decreased towards the median sulcus. The area postrema and the facial colliculus lacked cilia and were covered with non-ciliated ependymal cells. Along the entire length of the median sulcus supraependymal globular protrusions were seen. Over the rostral and middle thirds of the sulcus these protrusions exhibited interwoven ridges. At the former situation they were closely approximated but at the latter they were on the surface of non-ciliated nodules which were lying amongst sparsely ciliated cells. In the caudal third these protrusions presented smoother surfaces without any structural details over them. Transmission electron microscopy through the upper two thirds of the median sulcus revealed these surface protrusions to be non-ciliated cells having long and profuse network of interwoven microvilli over their luminal surface. These cell bodies exhibited well-defined supranuclear Golgi complexes, vesiculated rough and smooth surfaced endoplasmic reticulum, free ribosomes and polyribosomes, few electron dense granules, network of microtubules and light and dense multivesiculated bodies. These features suggested a secretory and/or absorptive role, rather that autophagy to these surface specialization.

Animals↗
PubMed2005

Dysfunctional cilia lead to altered ependyma and choroid plexus function, and result in the formation of hydrocephalus.

Cilia are complex organelles involved in sensory perception and fluid or cell movement. They are constructed through a highly conserved process called intraflagellar transport (IFT). Mutations in IFT genes, such as Tg737, result in severe developmental defects and disease. In the case of the Tg737orpk mutants, these pathological alterations include cystic kidney disease, biliary and pancreatic duct abnormalities, skeletal patterning defects, and hydrocephalus. Here, we explore the connection between cilia dysfunction and the development of hydrocephalus by using the Tg737orpk mutants. Our analysis indicates that cilia on cells of the brain ventricles of Tg737orpk mutant mice are severely malformed. On the ependymal cells, these defects lead to disorganized beating and impaired cerebrospinal fluid (CSF) movement. However, the loss of the cilia beat and CSF flow is not the initiating factor, as the pathology is present prior to the development of motile cilia on these cells and CSF flow is not impaired at early stages of the disease. Rather, our results suggest that loss of cilia leads to altered function of the choroid plexus epithelium, as evidenced by elevated intracellular cAMP levels and increased chloride concentration in the CSF. These data suggest that cilia function is necessary for regulating ion transport and CSF production, as well as for CSF flow through the ventricles.

Animals↗