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PubMedDate not supplied

[The polarization of neuroepithelial cells when a portion of the neural plate is inserted into the neural tube cavity in amphibian embryos].

Portions of homologous neuroepithelium of various length were introduced into the neural tube cavity in Rana arvalis and Pleurodeles waltlii late neurula. The neural tube in R. arvalis was destroyed independently of the transplant length. In P. waltlii neural primordia were deformed if a large transplant prevented closing of the neural tube. Redundant increase in the host cells length (polarization) was observed during the small transplant-induced retardation of neurulation. Recipient cells elongated 1.5-2 fold as compared to the normal ones. Zones of contact polarization were detected. They arise in slowly relaxing layer under conditions during the transplant-induced retardation of neurulation. The labelled TRITC cells introduced into the neural tube cavity integrated into the wall of the neural tube and retarded polarization of its cells.

Amphibians↗
PubMed1998

Effect of dexamethasone on cell proliferation of neuroepithelial tumor cell lines.

The effect of glucocorticoid on cell proliferation, the expression of glucocorticoid receptor, and the relationship between inhibition of cell growth and apoptosis were investigated in four established neuroepithelial tumor cell lines (KNS42, T98G, A172, and U251MG). Glucocorticoid receptor expression was located in the cytoplasm of untreated cells, but translocated into nuclei after treatment with dexamethasone in KNS42, T98G, and A172 cells. U251MG did not express glucocorticoid receptors. Dexamethasone significantly inhibited the growth of KNS42 and T98G cell lines, at high concentrations in contrast to growth stimulation at low concentration. Dexamethasone inhibited proliferation of A172 cell line at all concentrations from 10(-4) M to 10(-7) M. These were prevented by RU38486, a specific glucocorticoid antagonist. Apoptosis did not occur in any cell lines after dexamethasone treatment. There was no response to glucocorticoid by U251MG cells. Dexamethasone treatment of neuroepithelial tumor cells expressing glucocorticoid receptors causes translocation into the nucleus to modulate cell proliferation upon binding of different concentrations of dexamethasone in vitro. Dexamethasone inhibits proliferation of some neuroepithelial cell lines, not by glucocorticoid-induced apoptosis. The bimodal potential of glucocorticoid to stimulate or suppress proliferation of neuroepithelial tumor cells expressing glucocorticoid receptor must be considered in clinical trials.

Cell Division↗
PubMed2005

Glycosphingolipid synthesis inhibitor represses cytokine-induced activation of the Ras-MAPK pathway in embryonic neural precursor cells.

Neuronal and glial cells in the central nervous system are generated from common neural precursor cells during development. To evaluate the functions of glycosphingolipids (GSLs) in neural precursor cells, neuroepithelial cells (NECs) were prepared from mouse embryos (E14.5), and the effects of an inhibitor of glucosylceramide synthesis, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), on NECs was investigated. In PDMP-treated NECs, the expression of GD3, a major ganglioside of NECs, disappeared. We found that basic fibroblast growth factor (bFGF)-induced proliferation and extracellular signal-regulated kinase (ERK) activation were repressed in PDMP-treated NECs. Leukemia inhibitory factor (LIF)-induced ERK activation was also abolished in PDMP-treated NECs, suggesting that PDMP specifically represses the Ras-MAPK pathway. bFGF-induced activation of the Ras-MAPK pathway in NECs is dependent on GSL-enriched microdomains, lipid rafts. The organization of lipid rafts and the distribution of Ras and Grb2-SOS in the microdomains were not affected. However, Ras activation was repressed in PDMP-treated NECs. In PDMP-treated NECs, some neuronal genes were up-regulated and glial genes were down-regulated. These results suggest that GSLs might be involved in the proliferation, survival, signal transduction and differentiation of NECs.

Animals↗
PubMed1975

Functional morpho-histology of the alimentary canal of an Indian frewhwater major carp, Labeo rohita (Hamilton) during it's different life-history stages.

1. The alimentary canal of the fry of L. rohita (Hamilton) is of the carnivorous type in nature and disposition with a low relative length of the gut (R. L. G.). 2. End-buds are present. The buccopharyngeal region has a simple epithelial surface. Mucous cells are small and few throughout the length of the alimentary canal. The presence of these structures in association with a zooplankton feeding habit indicate that the fries are primarily sightfeeders and carnivorous. 3. With increase in age and body-length, the food and feeding habits of the fish undergo changes and accordingly the fingerlings and adults become herbivorous. The value of the R. L. G. steadily increases and the alimentary canal gradually develops into the typically herbivorous type. 4. Tast buds by now become completely developed and have lamina propria, sustentacular cells, neuroepithelial cells, gustatory pores and gustatory canals. 5. Taste buds are abundant in the lip, buccopharynx and anterior oesophagus. The buccopharyngeal region is also provided with distinct villi. Mucous cells are abundant and large being present throughout the alimentary canal. 6. The frequency, length, breadth and distribution of the mucous cells and taste buds are significantly different in marked contrast with those of the fry thus indicating that the fingerlings and adults depend primarily on their gustatory organs for feeding. The fingerlings and adults therefore, are herbivorous and tast feeders.

Animals↗
PubMedDate not supplied

Neurotoxicity of diphenylhydantoin (DPH) in the cerebellum of Mongolian gerbils--an enzyme histochemical study.

The influence of DPH on the cortex cerebelli of Mongolian gerbils was studied by cytochemical means in acute and chronic experiments. Liver specimens were investigated for comparative purposes. In the cellular elements of the cortex, such as Purkinje cells, neuroepithelial cells, and granule cells, DPH led to an activation of lysosome-bound enzymes and to a decrease of thiamine pyrophosphatase activity in Purkinje cells. Amino-peptidase A, occurring in the entire capillary network, was inhibited by DPH in vivo as well as in vitro. In the liver, however, no change of aminopeptidase A activity could be seen. Enzyme activity of aminopeptidase M and y-glutamyltranspeptidase in cerebellar vessels remained unaffected. Activity of y-glutamyltranspeptidase in the glia, however, increase considerably under the influence of DPH. While in the liver comparable enzymatic changes were most obvious in acute experiments, DPH induce the most distinct changes in the cerebellar cortex during chronic application. The neurotoxic effect of DPH on the cerebellum may on the one hand be due to lesions of the blood-brain barrier, probably only in the cerebellum, and on the other hand to the cerebellum specific relation between GABA metabolism and y-glutamyltranspeptidase activity.

Animals↗
PubMed1994

Differentiation and maturation of astrocytes derived from neuroepithelial progenitor cells in culture.

Neuroepithelial progenitor cells from striata of adult mice develop into either astrocytes or neurons when cultured in the presence of epidermal growth factor (B. A. Reynolds, and S. Weiss, Science 255: 1707-1710, 1992). We instituted primary cultures of such progenitor cells from forebrains of newborn rat pups in an epidermal growth factor-containing medium free of serum in order to study the development of astrocytes in culture. At 4-6 days, primary cultures consisted of floating clusters of proliferating cells which expressed nestin, a marker for neuroepithelial progenitor cells, the ganglioside GD3, and vimentin. When clusters were transferred to polylysine-coated dishes, cells attached to the substrate and began to express antigens characteristic of particular differentiated neurons, astrocytes, or oligodendrocytes within 2 weeks. In 4- to 6-week-old secondary cultures, levels of vimentin expression appeared to decrease within maturing astrocytes which had increased levels of glial fibrillary acidic protein. These results suggest that multipotential epidermal growth factor-progenitor cells can give rise to both neurons and macroglia of the adult central nervous system, and that maturation of the astrocytes in vitro may be occurring in a pattern similar to that seen in vivo. Furthermore, no glial fibrillary acidic protein-positive cells expressed the A2B5 antigen in the same cell indicating an absence of type-2 astrocytes.

Animals↗
PubMed1992

Nestin expression in embryonic human neuroepithelium and in human neuroepithelial tumor cells.

Nestin is a recently described member of the intermediate filament (IF) protein family that is especially abundant in neuroepithelial stem cells of the rat. The studies described here examine this class VI IF protein in the normal human developing central nervous system (CNS), human brain tumor-derived cell lines, and tissue samples of human CNS tumors. Human nestin exhibited biochemical and immunochemical properties similar to those of rat nestin. Further, as in the rat, nestin was detected immunohistochemically in several different types of immature human CNS cells, i.e. germinal matrix cells, neuroepithelial cells lining the central canal, radial glia and vascular cells. Nestin appeared in these cells at the earliest gestational age (i.e., 6 weeks) examined here and then it declined in all but the vascular cells at later embryonic stages. Nestin also was detected by immunocytochemistry in 6 of 7 primitive neuroectodermal tumor cell lines and in both of 2 malignant glioma cell lines examined. In these cell lines, nestin co-localized incompletely with bundles of IFs containing other IF proteins (i.e., vimentin, glial filament, neurofilament). Nestin was ubiquitous in a wide variety of brain tumors, but was most prominent in gliomas. The transient expression of nestin in primitive neuroepithelial cells at early stages of human embryogenesis and its abundance in neuroepithelial tumors suggest a role for nestin IFs in cellular events that precede the exit of embryonic CNS stem cells from the cell cycle and the commitment of the progeny of these stem cells to a specific lineage. The subsequent induction of different members of the IF protein family in phenotypically distinct CNS cells (i.e. neurons, glia) and the elimination of nestin from almost all differentiated CNS cells, imply that different classes of IFs subserve functions that are closely linked to the maturational state, as well as the lineage, of CNS cells.

Adolescent↗
PubMed1998

Measles virus infection and replication in undifferentiated and differentiated human neuronal cells in culture.

Measles virus (MV) infection of the human central nervous system (CNS) typically involves widespread infection of neurons. However, little is known about how they become infected, how defective virus arises and accumulates, or how virus spreads among the cells of the CNS. In vitro studies of viral interactions with human neuronal cells may contribute to the resolution of such issues. In mixed cultures containing differentiated human neuronal (hNT2) cells and neuroepithelial cells, immunofluorescence studies show that the neurons, unlike both their NT2 progenitors and the neuroepithelial cells, are not initially susceptible to MV infection. This is possibly due to their lack of expression of CD46, a known cell surface receptor for MV. Later in the course of infection, however, both MV proteins and genomic RNA become detectable in their processes, where they contact infected, fully permissive neuroepithelial cells. Such a mechanism of virus transfer may be involved in the initiation and spread of persistent MV infection in diseases such as subacute sclerosing panencephalitis. Furthermore, mutated defective virus may readily accumulate and spread without the need, at any stage, for viral maturation and budding.

Cell Differentiation↗
PubMed1980

The ultrastructural characteristics of the apical cell in the neuroepithelial bodies of the toad lung (Bufo marinus).

The cytological features and membrane specialisations of neuroepithelial cells (apical cells) in direct contact with the lumen of the lung were studied with transmission and scanning electron microscopy. The luminal surface of the apical cell is characterised by microvilli, a cilium with an 8 + 1 microtubular pattern and numerous coated vesicles. The cytoplasmic region immediately beneath the luminal plasma membrane contains numerous smooth-walled vesicles, tubules and microtubules, a few microfilaments and dense granules (15-20 nm in diameter). The luminal pole of the cell is marked off from the basal or vascular pole by a well-defined terminal web associated with junctional complexes. Protrusion of the luminal pole occurs as a transient phenomenon and is accompanied by a pinching in of the cell at the terminal web. It is proposed that the distinctive features of the luminal pole of the apical cell are comparable to those of recognised chemoreceptor cells. It is also proposed that in view of the common features of apical and basal cells the apical cell functions as a receptor/transducer and the basal cells served as an accessory source of peptides/5-hydroxytryptamine to be released on stimulation of the apical cell. Furthermore, we have drawn attention to the structural heterogeneity of the neuroepithelial bodies in various vertebrate classes.

Animals↗
PubMed2006

FGF2 plays a key role in embryonic cerebrospinal fluid trophic properties over chick embryo neuroepithelial stem cells.

During early stages of brain development, neuroepithelial stem cells undergo intense proliferation as neurogenesis begins. Fibroblast growth factor 2 (FGF2) has been involved in the regulation of these processes, and although it has been suggested that they work in an autocrine-paracrine mode, there is no general agreement on this because the behavior of neuroepithelial cells is not self-sufficient in explants cultured in vitro. In this work, we show that during early stages of development in chick embryos there is another source of FGF2, besides that of the neuroepithelium, which affects the brain primordium, since the cerebrospinal fluid (E-CSF) contains several isoforms of this factor. We also demonstrate, both in vitro and in vivo, that the FGF2 from the E-CSF has an effect on the regulation of neuroepithelial cell behavior, including cell proliferation and neurogenesis. In order to clarify putative sources of FGF2 in embryonic tissues, we detected by in situ hybridization high levels of mRNA expression in notochord, mesonephros and hepatic primordia, and low levels in brain neuroectoderm, corroborated by semiquantitative PCR analysis. Furthermore, we show that the notochord segregates several FGF2 isoforms which modify the behavior of the neuroepithelial cells in vitro. In addition, we show that the FGF2 ligand is present in the embryonic serum; and, by means of labeled FGF2, we prove that this factor passes via the neuroepithelium from the embryonic serum to the E-CSF in vivo. Considering all these results, we propose that, in chick embryos, the behavior of brain neuroepithelial stem cells at the earliest stages of development is influenced by the action of the FGF2 contained within the E-CSF which could have an extraneural origin, thus suggesting a new and complementary way of regulating brain development.

Animals↗
PubMed2004

Hes genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation.

Radial glial cells derive from neuroepithelial cells, and both cell types are identified as neural stem cells. Neural stem cells are known to change their competency over time during development: they initially undergo self-renewal only and then give rise to neurons first and glial cells later. Maintenance of neural stem cells until late stages is thus believed to be essential for generation of cells in correct numbers and diverse types, but little is known about how the timing of cell differentiation is regulated and how its deregulation influences brain organogenesis. Here, we report that inactivation of Hes1 and Hes5, known Notch effectors, and additional inactivation of Hes3 extensively accelerate cell differentiation and cause a wide range of defects in brain formation. In Hes-deficient embryos, initially formed neuroepithelial cells are not properly maintained, and radial glial cells are prematurely differentiated into neurons and depleted without generation of late-born cells. Furthermore, loss of radial glia disrupts the inner and outer barriers of the neural tube, disorganizing the histogenesis. In addition, the forebrain lacks the optic vesicles and the ganglionic eminences. Thus, Hes genes are essential for generation of brain structures of appropriate size, shape and cell arrangement by controlling the timing of cell differentiation. Our data also indicate that embryonic neural stem cells change their characters over time in the following order: Hes-independent neuroepithelial cells, transitory Hes-dependent neuroepithelial cells and Hes-dependent radial glial cells.

Animals↗
PubMed1976

Selective lethal effect of supranormal temperatures on human neoplastic cells.

The effects of supranormal temperatures upon normal human cells (derived from normal adult and embryonal tissues) and neoplastic human cells (derived from biopsies of malignant tumors) have been quantitatively studied in tissue culture. Melanoma cells have been compared with melanocytes derived from fetal uveas. Colon carcinoma cells have been compared with embryonal intestinal epithelial cells. Malignant neuroepithelial cells derived from a teratocarcinoma of the ovary have been compared with neuroepithelial cells derived from fetal brain. Fibrosarcoma cells have been compared with normal adult fibroblasts. All cells defined as neoplastic have produced malignant tumors when injected into nude thymus-deficient mice at doses of 1 X 10(7) cells or less. Exposure to temperatures of 42.5-43.0 degrees for 4 to 8 hr has been shown to have significantly greater lethal effect on the tumor cells than on the nonneoplastic cells.

Carcinoma↗
PubMed1995

Evidence for multiple precursor cell types in the embryonic rat cerebral cortex.

Cell lineage studies of the rat cerebral cortex suggest that by midneurogenesis, most precursor cells of the ventricular zone are specified to produce a single cell type. Yet there is also evidence for multipotential precursor cells. We used a retroviral vector to follow the developmental potential of cortical precursor cells by labeling cortical cells in cultures from embryos between 12 and 18 days of gestation. We found specified precursor cells as early as embryonic day 12, in addition to bipotential cells that generate neurons and astrocytes. Most importantly, we discovered a type of neural precursor cell, a neuroepithelial cell, that predominates earlier in development, differs distinctly from the specified precursor cells, and as a population, appears to be multipotential. These data suggest that corticogenesis progresses from an early phase dominated by neuroepithelial cells to a later phase characterized by multiple populations of specified precursor cells.

Animals↗
PubMed1987

Shaping of the chick neuroepithelium during primary and secondary neurulation: role of cell elongation.

Cell elongation is a cardinal event in formation and shaping of the neuroepithelium during both primary and secondary neurulation. This study had three purposes. The first was to clarify the role of microtubules in maintaining the elongated configurations of chick neuroepithelial cells. Neuroepithelial cells of the neural plate (the rudiment of the primary neural tube) and medullary cord (the rudiment of the secondary neural tube) reduced their heights an average of approximately 25% when their microtubules were depolymerized, but most cells remained considerably elongated and columnar. Complete rounding up occurred only as cells entered metaphase where they arrested. These results suggest that microtubules as well as other factors are required to maintain the fully elongated configurations of cells composing epithelial sheets. The second purpose of this study was to evaluate the hypothesis that neuroepithelial cell elongation plays a major role in narrowing of the neural plate. To do this, the width of the neural plate was examined after microtubule depolymerization and repolymerization. As the heights of neuroepithelial cells decreased with loss of their microtubules, the width of the neuroepithelium increased roughly proportionately; subsequent repolymerization with concomitant cell elongation resulted again in neural plate narrowing. Thus, the hypothesis is supported. The third purpose of this study was to examine the roles of cell rearrangement and change in neuroepithelial cell or extracellular volume in neural plate narrowing and extension. Extensive cell rearrangement, resulting in net cell loss from the width of selected, representative levels of the neural plate, does not seem to play a major role in plate narrowing, but decreases in cell or extracellular volume are likely involved. Further studies are necessary to complete our understanding of the mechanisms driving neural plate shaping and bending.

Animals↗
PubMed1995

Neuroepithelial progenitor cells explanted from human fetal brain proliferate and differentiate in vitro.

Putative neuroepithelial cells were explanted from several germinative zones of the brain of 5-to-12 week old human fetuses, obtained from legal abortions. In each case, an homogeneous population of neuroepithelial-like cells expressing nestin and vimentin was obtained. Cells proliferated in vitro in response to bFGF which favoured a neuroblastic differentiation with expression of MAP-5 and beta3-tubulin. Cells could be maintained and propagated as neuroblasts in serum-free medium. The multipotentiality of the cells was revealed by growing them in serum-containing medium, where a mixed population of cells of the neuronal lineage and of glial cells including putative radial glia, astrocytes and oligodendrocytes, progressively differentiated. These human progenitor cells proliferating in vitro have many potential applications in gene therapy of neurodegenerative diseases.

Brain↗