[Ventricular topography of the diencephalic ependyma in Rattus rattus (L.)--a scanning electron microscopy study].
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1-day-old postnatal rats were given daily intraperitoneal injections of chloroquine for 6 successive days and sacrificed at 7, 14 and 21 days of age. In rats killed at 7 and 14 days of age, the choroid plexus epithelial cells and ependymal cells lining the lateral ventricles showed a marked increase in number and size of lysosomes; some cells were extremely vacuolated. The epiplexus cells associated with the choroid plexus were also affected showing numerous vacuoles and lamellar bodies. Furthermore, their immunoreactivity with the antibodies OX-42, OX-18, OX-6 and ED1 were augmented when compared with cells in the control rats. At 21 days of age the ultrastructural features of the various cell types in the chloroquine-injected rats resembled those in the corresponding control rats. The immunoreactivity of epiplexus cells was also comparable in the two groups of animals at this time point. It is concluded from this study that although chloroquine induces acute structural alterations of choroid plexus epithelial cells, ependymal cells and epiplexus cells, its effects are reversible since the cells regained their normal ultrastructure and immunohistochemical features following the discontinuation of the drug.
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A survey of the literature shows that proliferation of ependyma occurs largely during the embryonic and early postnatal periods of development in most species. Differentiation of these cells proceeds along particular regional and temporal gradients as does the expression of various cytoskeletal (vimentin, cytokeratins, glial fibrillary acidic protein) and secretory proteins (S-100). Turnover declines significantly postnatally, and only low levels of residual activity persist into adulthood under normal conditions. Although the reported response of ependyma to injury is somewhat equivocal, only limited regenerative capacity appears to exist and to varying degrees in different regions of the neuraxis. Proliferation has been most often observed in response to spinal cord injury. Indeed, the ependyma plays a significant role in the initiation and maintenance of the regenerative processes in the spinal cord of inframammalian vertebrates. In the human, however, ependyma appears never to regenerate at any age nor re-express cytoskeletal proteins characteristic of immature cells. The functions of ependyma including tanycytes, a specialized form of ependymal cell that persists into adulthood within circumscribed regions of the nervous system, are still largely speculative. Fetal unlike mature ependyma is believed to be secretory and is believed to play a role in neurogenesis, neuronal differentiation/axonal guidance, transport, and support. In the adult brain, mature ependyma is not merely an inert lining but may regulate the transport of ions, small molecules, and water between the cerebrospinal fluid and neuropil and serve an important barrier function that protects neural tissue from potentially harmful substances by mechanisms that are still incompletely understood.
The fine structure of the parvocellular tuberal nuclei and that of the ependyma bordering the third ventricle in the basal hypothalamus of the White-crowned Sparrow, Zonotrichia leucophrys gambelii, have been investigated. Photoperiodically stimulated birds have been compared with birds held on short days. The perikarya of the neurons of the basal infundibular (tuberal) nucleus, and in part, of the more dorsal layers, contain dense-cored granules (1000-1500 A). The granules in the anterior part of the nucleus are somewhat larger than those of the posterior part. The synapses and the synaptic relationships of these cells are described. The single-layered ependyma of the third ventricle in the basal hypothalamus may be divided into the dorsal typical ependyma, the ventrolateral "glandular" ependyma, and the ventral "glandular" ependyma. Cells of the ventral ependyma lack apical cilia but bear a few microvillous processes. They have well-developed Golgi apparatus, conspicuous polysomes, and frequently dense, irregularly-shaped granules. Basal cytoplasmic processes extend ventrally to the outer surface of the median eminence. Photoperiodic stimulation appears to increase the numbers of apical protrusions of the cells in the ventral glandular ependyma and to cause an increase in size of the nerve cells of the basal infundibular nucleus.
In the subcommissural organ (SCO) of the guinea pig, rat, golden hamster, and mouse the activity and distribution of enzymes related to the energy-supplying metabolism and of some marker enzymes of different cell organelles have been investigated by means of mostly modified histochemical methods. The results were compared with findings in the ciliated ependyma of the ventricular wall and with those in the ependyma of the choroid plexus of the third ventricle. In the ependymal part of the SCO only a moderate activity of hexokinase is observed in its specialized columnar cells whereas a high activity is present both in the ciliated ependyma and the choroid plexus. - The staining pattern of glucose-6-phosphatase is similar to that of hexokinase but this enzyme is found is the SCO only. - Likewise hexokinase, glycogen granules and enzymes related to glycogen metabolism (phosphoglucomutase, uridine-diphosphoglucose pyrophosphorylase, glycogen synthetase and phosphorylase) are regularly found most numerous and active in the nuclear and supra-nuclear area of the ependymal part. These enzymes are less active in both the other ependymal regions. - Uridine-diphosphoglucose dehydrogenase could not be demonstrated in the SCO. The NADP-linked enzymes of the pentose phosphate shunt, glucose-6-phosphate and 6-phosphogluconate dehydrogenase, show a moderate activity which decreases also from the nuclear towards the apical area of the ependymal cells of the SCO. Enzymes of the glycolytic pathway, such as glucosephosphate isomerase, fructose-6-phosphate kinase, fructose-I,6-diphosphate aldolase, glyceraldehyde-3-phosphate and lactate dehydrogenase, are highly active in the SCO and are located mainly in the supranuclear area, too. Fructose-1,6-diphosphatase could not be demonstrated thus indicating that in the SCO the pathway is most probably only glycolytic but not gluconeogenetic. Compared to the ependyma of the ventricular wall and of the choroid plexus, in the SCO the M type subunits of lactate dehydrogenase predominate. Glycolytic enzymes are also very active in the choroid plexus but less in the ciliated ependyma. Compared to the ciliated ependyma and especially to the ependyma of the choroid plexus, the activities of enzymes which are only present in mitochondria (NAD-linked isocitrate dehydrogenase, succinate dehydrogenase, NAD-linked malate dehydrogenase after preextraction, cytochrome oxidase, 3-hydroxybutyrate and glycerolphosphate and glutamate dehydrogenase) are relatively low. Mitochondria are accumulated near the superior pole of the nuclei as well as in the most apical part of the ependymal cells. - The staining pattern of NADP-linked isocitrate and malate dehydrogenase as well as of NADH dehydrogenase suggests that these enzymes are localized both in and out of mitochondria. The extramitochondrial activity of the first two enzymes might be localized in the cytosol. The extramitochondrial activity of NADH dehydrogenase might be localized in the endoplasmic reticulum...
Absorption, accumulation and release of N-Dansyl-L-phenylalanine (DPA) through the ependyma, plexus choriodei and brain parenchyma after intraventricular and intracisternal injection was examined at different postinjection intervals by fluorescence microscopy. The following results were obtained: 1. After intraventricular injection, DPA is rapidly absorbed from the ependyma and plexus choriodei in all ventricles and subsequently disappears from the various points of the ventricles at different times. DPA is no longer evident in the ependyma after 40 min and the plexus after 90 min. Aborption and storage occur primarily in the dopaminergic centers of the brain. This stage begins 5 min p.i. attains a maximum after 40 min and is maintained up to 180 min p.i. 2. If DPA is administered intracisternally, fluorescence is initially restricted to the ependyma and choroid plexus of the fourth ventricle and to the wall of the aquaeduct. Only at 5-10 min p.i. are rostral ventricular portions labelled. Passage of the amino acid out of the ventricle only occurs to a limited extent. 40 min after intracisternal injection, DPA is no longer demonstrable in the ependyma and plexus or brain parenchyma. 3. Intrathecally administered DPA appears in the periglomerular tubules of the kidney as well 2.5 min p.i. and is stored there for up to 40 min. The kidney medulla remains free of fluorescence. 4. DPA injected into the CSF is protein-bound.
The ependyma was examined in eight children with neuroblast migratory disorders of diverse origin: three cases of lissencephaly type 1 with severe to mild degrees of agyria/pachygyria, four cases of lissencephaly type 2 in Fukuyama muscular dystrophy and the Walker-Warburg syndrome, and one case of hemimegalencephalic pachygyria. Morphological and immunohistochemical abnormalities of the ependyma were strikingly similar in all. Discontinuities were disproportionate to the degree of ventriculomegaly. In some regions, the ependyma remained a pseudostratified columnar epithelium, though basal processes were absent. The poles of the horns of the lateral ventricles were replaced by extensive heterotopic ependymal rosettes. Rosettes and rows of ependyma also were in other subventricular sites. Subependymal nodules of large astrocytes and their processes bulged into the ventricular lumen after infancy. Ependymal cells did not express glial fibrillary acidic protein, but showed persistent expression of S-100 protein, cytokeratin CK-904 and sometimes vimentin long after these proteins normally disappear. An abnormal ependyma in lissencephaly/pachygyria may contribute to disturbances in neuronogenesis, guidance of axonal projections and neuroblast migrations; it may be a primary factor in pathogenesis.