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PubMed1998

Emigration of neuroepithelial cells from the hindbrain neural tube in the chick embryo.

It is generally believed that after the emigration of neural crest, the neuroepithelial cells of the neural tube are committed to differentiate only as neurons and supporting cells of the central nervous system. Neural crest cells arise from the dorsal portion of the developing neural tube and contribute to the formation of the peripheral nervous system and a variety of non-neural structures. In contrast to this view we have recently shown, by focal application of the vital dye Dil in duck embryos, that an additional population of cells emigrates from the neural tube. By using an entirely different technique we confirm and extend these observations in the chick embryo. Replication-deficient retroviral vector LZ12 containing the gene LacZ was utilized to label the neural tube cells. The viral concentrate was microinjected into the lumen of the rostral hind-brain neural tube, considerably after the completion of emigration of neural crest cells. The labeled cells were monitored in whole mounts and histological sections. Initially, the labeled cells were restricted to the neuroepithelium of the hindbrain neural tube. Subsequently, they were seen in the neural tube and in the ganglion of the fifth cranial nerve (trigeminal ganglion). Later, they migrated beyond the trigeminal ganglion, i.e., into the mesenchyme of the first pharyngeal arch. Immunostaining with the neural crest cell marker, HNK-1, indicated that the emigrated neuroepithelial cells were HNK-1 negative. It is concluded that in the chick embryo some neuroepithelial cells emigrate at the site of attachment of the trigeminal nerve, migrate into the ganglion and then into the mesenchyme of the first arch. This cell population differs antigenically from the neural crest cells.

Animals↗

PubMed2001

Ephrin B1 is expressed on neuroepithelial cells in correlation with neocortical neurogenesis.

To identify molecules involved in neurogenesis, we have raised monoclonal antibodies against embryonic day 12.5 mouse telencephalon. One antibody, monoclonal antibody 25H11, stains predominantly the ventricular zone of the anterior and lateral telencephalon. Purification of the 25H11 antigen, a 47 kDa integral membrane protein, from approximately 2500 mouse telencephali reveals its identity with ephrin B1. Ephrin B1 appears at the onset of neocortical neurogenesis, being first expressed in neuron-generating neuroepithelial cells and rapidly thereafter in virtually all neuroepithelial cells. Expression of ephrin B1 persists through the period of neocortical neurogenesis and is downregulated thereafter. Ephrin B1 is present on the ventricular as well as basolateral plasma membrane of neuroepithelial cells and exhibits an ventricular-high to pial-low gradient across the ventricular zone. Expression of ephrin B1 is also detected on radial glial cells, extending all the way to their pial endfeet, and on neurons in the mantle/intermediate zone but not in the cortical plate. Our results suggest that ephrin B1, presumably via ephrin-Eph receptor signaling, has a role in neurogenesis. Given the ventricular-to-pial gradient of ephrin B1 on the neuroepithelial cell surface and its known role in cell migration in other systems mediated by its repulsive properties, we propose that ephrin B1 may be involved in the migration of newborn neurons out from the ventricular zone toward the neocortex.

Animals↗

PubMed1995

An immortalized mouse neuroepithelial cell line with neuronal and glial phenotypes.

Evidence from retroviral marking techniques and immortalized cell lines indicates that multipotential stem cells exist in many areas of the developing central nervous system. However, the factors that influence the commitment of these stem cells into distinct neuronal or glial lineages are not known. We have created an immortalized hypothalamic cell line derived from embryonic day 14 hypothalamic cells with a replication-defective retroviral construct containing a temperature-sensitive allele (tsA58) of the large T antigen of the simian virus 40. The clonality of this cell line, which we have named V1, was established by single cell cloning and by Southern blot analysis. V1 cells exhibit two different morphologies: the vast majority of cells are flat and stellate, and a smaller number are phase-bright round cells with processes. V1 cells express nestin and neural-cell adhesion molecule, typical of proliferating neuroepithelial cells. They also express glial fibrillary acidic protein and S100 as well as the low molecular weight neurofilament protein. In addition, the phase-bright, process-bearing V1 cells stain intensely for many typical neuronal proteins, such as low, medium and high molecular weight neurofilament proteins, tau protein, microtubule-associated protein-2, and neuron-specific enolase. The phase-bright cells also have condensed chromatin and display mitotic spindles, indicating that they are in mitosis. When V1 cells are transferred from the permissive temperature (33 degrees C) to the restrictive temperature (39 degrees C), there is a decrease in expression of NF-L and an increase in expression of NF-H and glial fibrillary acidic protein in the flat V1 cells. The enhanced expression of neuronal antigens in mitotically active V1 cells is novel and may represent a more general property of the differentiation process. We suggest that V1 cells arise from a mixed neural/glial neuroepithelial progenitor cell that expresses both neuronal- and glial-specific proteins in the developing hypothalamus.

Animals↗

PubMed2000

Astrocyte differentiation of fetal neuroepithelial cells by interleukin-11 via activation of a common cytokine signal transducer, gp130, and a transcription factor, STAT3.

The interleukin (IL)-6 family cytokines utilize membrane glycoprotein gp130 in common as a critical signal-transducing receptor component. IL-11, a cytokine initially identified as a plasmacytoma growth factor, belongs to this family. We show here that IL-11 and its cognate receptor components are expressed in fetal mouse neuroepithelial cells. We also show that after 4 days of culture with IL-11, cells with typical astrocytic morphologies expressing glial fibrillary acidic protein (GFAP; a marker for astrocytes) come out. This differentiation process is totally dependent on the gp130-mediated signal-transduction pathway involving activation of a latent cytoplasmic transcription factor, STAT3 (for signal transducer and activator of transcription 3), because (a) IL-11-induced astrocyte differentiation is not observed when neuroepithelial cells prepared from gp130-deficient mice were used, (b) stimulation of neuroepithelial cells by IL-11 rapidly induces tyrosine-phosphorylation of STAT3, and (c) transfection of neuroepithelial cells with a dominant-negative form of STAT3 inhibits IL-11-induced activation of the GFAP gene promoter. We have further identified, in the GFAP promoter region, a STAT3 site at which nucleotide substitutions almost completely abolished the IL-11-induced GFAP promoter activation. Taken together, it is suggested that IL-11 contributes to astrocytogenesis in fetal brain via activation of gp130 and STAT3.

Animals↗

PubMed2003

Progressive restriction of cell fates in relation to neuroepithelial cell mingling in the mouse cerebellum.

Neurogenesis in the cerebellum proceeds through a temporal series of cell production from two separate epithelia, the ventricular zone (VZ) and the external granule cell layer (EGL). Using the laacZ cell lineage tracer in transgenic mice, we describe cellular clones whose dates of birth span the entire period of cerebellar development and deduce a sequence of cell dispersion leading to the final allocation of cells in the cerebellum. Clones probably labeled early during neural tube formation show that individual progenitors can give rise to all cerebellar cell types. The distribution of clonally related granule cells in these clones indicates a mediolateral organization of EGL progenitors already established before the allocation of the EGL progenitors to the cerebellum. Clones restricted to the cerebellar VZ show that the VZ derives progenitors for deep nuclei and multipotent cortical progenitors, which lose their systematic lineage relationship when longitudinal cell intermingling in the cerebellar VZ becomes more limited. The small clones also show that cell dispersion is radial in the internal granule layer and tangential in the molecular layer. Together, the data demonstrate the broad maintenance of the relative order of cells from neural tube stages to the adult cerebellum.

Animals↗

PubMed1996

A novel tetrodotoxin-resistant sodium current from an immortalized neuroepithelial cell line.

1. Voltage-gated ionic currents were recorded from cells of an immortalized neuroepithelial cell line named V1. The cell line was produced by insertion of the temperature-sensitive tsA58 allele of the SV40 large T-antigen into embryonic day 14 mouse hypothalamic cells. V1 cells display a mixed immature neural-glial phenotype and have two phenotypes, round and flat. 2. Recordings from round V1 cells demonstrate voltage-gated Na+ and K+ currents (n = 297), while no voltage-gated currents were observed in flat V1 cells (n = 45). Voltage-gated currents were recorded from cells cultured at both permissive and restrictive temperatures. 3. Internal Cs+ and external tetraethylammonium (TEA) were used to suppress outward currents. The remaining inward current has rapid activation and inactivation time constants which decreased as the test potential increased. In different cells, the amplitude of the peak inward current varied from about 50 pA to as large as 4500 pA (in 120 mM external Na+). The reversal potential for the inward current was close to the predicted Nernst equilibrium potential for Na+. Both the magnitude and reversal potential of the inward current were dependent on the external Na+ concentration. It is therefore considered to be a Na+ current, INa. 4. INa was found to be TTX resistant. About 5% of the INa was blocked by 200 nM TTX and 20 microM TTX fully suppressed the Na+ current. The apparent Kd for TTX blockade was estimated to be 1.49 microM. 5. The activation kinetics of INa could be described by a Hodgkin-Huxley model with an m3 variable. The time constants of activation and inactivation of INa are fast, similar to those of the TTX-resistant and TTX-sensitive Na+ currents in central nervous system neurons and glial cells. 6. The divalent and trivalent cations Cd2+, Co2+, Ni2+, Zn2+ and La3+ shifted the activation of INa to more positive potentials and decreased the maximal conductance in a dose-dependent manner. The apparent Kd values for blockade of the INa by Cd2+, Co2+, Ni2+, Zn2+ and La3+ were 430, 3500, 1900, 83 and 202 microM, respectively. 7. The addition of phorbol myristate acetate, an activator of protein kinase C, consistently produced a reduction in the amplitudeof INa without affecting the time course of activation or inactivation. 8. INa in V1 cells expresses a unique combination of voltage and time kinetics and sensitivity to blockade by TTX and cations. We hypothesize that this Na+ current may be expressed transiently during development of the central nervous system at the stage of development represented by the V1 cell line.

Animals↗

PubMed1977

Ultrastructural alterations in neuroepithelial cells of mouse embryos exposed to cytotoxic doses of hydroxyurea.

Developing neuroepithelial cells from the cranial region of neural folds were examined at various intervals from 15 minutes to four hours after administration of teratogenic (250 mg/kg) or embryolethal (500 mg/kg) doses of HU to ICR/DUB mice on ninth day of gestation. Thirty percent of surviving fetuses showed extencephaly after the teratogenic dose. The initial ultrastructural change in some neuroepithelial cells occurred within 15 minutes to one hour after treatment with the teratogenic dose and involved a breakdown of polyribosomes into monosomes which were dispersed evenly in the cytosome. At one to two hours, condensation of the cytoplasm and chromatin was observed along with distorted nuclear shape. At two to four hours, cells exhibited extremely condensed cytoplasm and fragmentation of the cells occurred. The affected cells showed pyknotic nuclei and segregation of fibrillar and granular components of the nucleolus. In some nuclei, particularly after treatment with the higher dose of HU, a condensation of the nucleolus was observed. At this stage images were obtained which indicated that neighboring cells phagocytosed the cellular fragments derived from the HU affected cells.

Abnormalities, Drug-Induced↗

PubMed2003

A 90-degree rotation of the mitotic spindle changes the orientation of mitoses of zebrafish neuroepithelial cells.

In the neural plate and neural tube in the trunk region of the zebrafish embryo, dividing cells are oriented parallel to the plane of the neuroepithelium, while in neural keel/rod, cells divide perpendicular to it. This change in the orientation of mitosis is brought about by a 90 degrees rotation of the mitotic spindle. As the two halves of the neural primordium in keel/rod stage are in apposition, the perpendicular orientation of mitoses in this stage determines that daughter cells become allocated to both sides of the neural tube. To assess the role played by cell junctions in controlling the orientation of dividing cells, we studied the expression of components of adherens and tight junctions in the neuroepithelial cells. We find that these proteins are distributed irregularly at the neural plate stage and become polarised apically in the cell membrane only during the keel/rod stage. The stereotypic orientation of mitoses is perturbed only weakly upon loss of function of the cell junction components ASIP and aPKClambda, suggesting that mitotic orientation depends in part on the integrity of cell junctions and the polarity of the epithelium as a whole. However, the 90-degree rotation of the spindle does not require perfectly polarised cell junctions between the neuroepithelial cells.

Animals↗

PubMed1991

A method for the isolation of purified murine neuroepithelial cells from the developing mouse brain.

The adult mammalian central nervous system develops from the pseudostratified neuroepithelium of the neural tube. In order to study, in vitro, the differentiation of the neuroepithelial cells in detail and to identify factors that may influence this process, an uncontaminated, viable population of neuroepithelial cells, that still retains full developmental potential, is required. In this paper we describe a highly efficient method, involving differential trypsinization and micro-dissection, to cleanly separate the neuroepithelium from surrounding mesenchyme and ectoderm. The purity of isolated neuroepithelium has been assessed by monitoring for the presence of endothelial cells using an anti-endothelial antibody, MTS-12, and found to contain no significant level of contamination. Neuroepithelial cells prepared by this method have been demonstrated to divide and differentiate in tissue culture, to act as target cells for immortalization by proto-oncogenes and to differentiate into neurons in neural transplantation studies.

Animals↗

PubMed1982

Small-cell neuroepithelial tumor of skin: a Merkel-cell neoplasm?

Two patients with small-cell undifferentiated neuroepithelial tumors of skin are reported. The histologic and ultrastructural features of this neoplasm are presented. Characteristic membrane-bound, dense-core neurosecretory granules were seen in the cytoplasm of the tumor cells in both cases. The literature is reviewed in regard to the clinical behavior of these lesions and their possible cell of origin. Dermatologists should be aware of these tumors because they may require electron microscopy for accurate diagnosis. The tumors should be treated aggressively to minimize the chance of local recurrence and nodal or visceral metastases.

Aged↗

PubMed1997

Neuroepithelial cells downregulate their plasma membrane polarity prior to neural tube closure and neurogenesis.

Cell differentiation often involves changes in cell polarity. In this study we show that neuroepithelial cells, the progenitors of all neurons and macroglial cells of the vertebrate central nervous system, downregulate the polarized delivery to the apical and basolateral plasma membrane domains during development. Upon infection of the neuroepithelium of mouse embryos with fowl plague virus (FPV), polarized delivery of the viral envelope hemagglutinin, an apical marker, occurred at the neural plate stage (E8), but was downregulated at the open neural tube stage (E9). Upon infection with vesicular stomatitis virus, the viral envelope G protein, a basolateral marker, showed an unpolarized delivery not only at the open neural tube stage, but already at the neural plate stage. These results show that a progressive downregulation of plasma membrane polarity of neuroepithelial cells precedes neural tube closure and the onset of neurogenesis.

Animals↗

PubMed1990

Neural tube formation in the mouse: a morphometric and computerized three-dimensional reconstruction study of the relationship between apical constriction of neuroepithelial cells and the shape of the neuroepithelium.

Morphometry and computerized three-dimensional reconstruction were used to study the relationship between apical constriction of neuroepithelial cells and the pattern of bending of the neuroepithelium in the developing neural tube of the 12-somite mouse embryo. The neuroepithelium of the mouse exhibits prominent regional variations in size and shape along the embryo axis. The complex shape of most of the cephalic neural tube (e.g., forebrain and midbrain) is due to the coexistence of concave and convex bending sites whereas more caudal regions (e.g., hindbrain and spinal cord) generally lack sites of convex bending and have a relatively simple shape. The apical morphology of neuroepithelial cells was found to be correlated more closely with the local status of bending of the neuroepithelium than with the specific region of the neural tube in which they are located. In areas of enhanced apical constriction, microfilament bundles were particularly prominent. Morphometry revealed that patterns of bending of the neuroepithelium were correlated almost exactly with those of apical constriction throughout the forming neural tube. These findings support the idea that apical constriction of neuroepithelial cells, resulting from tension generated by microfilament bundles, plays a major role in bending of the neuroepithelium during neural tube formation in the mouse.

Actin Cytoskeleton↗

PubMed1996

Laminin-1 selectively stimulates neuron generation from cultured retinal neuroepithelial cells.

Signals derived from the extracellular matrix (ECM) largely influence neuron differentiation and development. However, the action of specific ECM components in these processes is poorly understood. This had led us to investigate the role of different laminins in the survival, proliferation, and neuron differentiation of cultured neuroepithelial cells from the developing chicken retina. Dissociated retinal neuroepithelial cells from 5-day-old chicken embryos, cultured on laminin-1, survived, proliferated, and differentiated into neurons, as assessed by both [3H]-thymidine uptake and acquisition of neuronal markers. Nevertheless, these effects took place only in the presence of cell-cell contact. In contrast, RN22 Schwannoma-derived laminin (devoid of alpha 1 chain) and merosin (bearing an alpha 2 chain), which also promoted proliferation when cell-cell contact occurred, led to reduced cell survival and failed to foster neuron differentiation. Furthermore, the laminin-1 P1 fragment (containing the rod-like portions of the short arms of the molecule) also failed to support neuron generation. In contrast, the laminin-1 E8 fragment (containing the long arm of the molecule) supported such a process to the same extent as the whole laminin-1 molecule, although a similar activity cannot be ruled out in other globular domains of the short arms. However, these results stress the importance of the carboxy-terminal part of alpha 1 chain in neuronal development. A cDNA fragment of a chicken alpha 1 chain was cloned and semiquantitative PCR amplification revealed that its mRNA is expressed in retinal neuroepithelial cells at the time of neuron differentiation. Our data strongly suggest that an alpha 1-like chain-containing laminin is needed for differentiation of neuron precursor cells.

Amino Acid Sequence↗

PubMed1987

Intracellular distribution of yolk droplets, lipid bodies and Golgi apparatus in the chick neuroepithelial cells during neurulation.

Vitelline and lipidic inclusions which are present in the neuroepithelial cells during chick embryo neurulation show a typical intracellular localization in the apical zone of the cell. In the same cellular zone the Golgi apparatus can be seen during the successive stages of neurulation. These patterns of inclusion and organelle polarity during chick embryo neurulation may be related to active consumption of the reserves contained in inclusions during this morphogenetic process. Such an active consumption would imply a close relationship between the vitelline and lipidic inclusions and the Golgi apparatus. On the other hand, the apical position of the Golgi apparatus in the neuroepithelial cells reveals the remarkable apicobasal polarity of these cells which remains unchanged during chick embryo neurulation.

Animals↗

PubMed1990

Neuroepithelial cell contacts in 12 days old rat embryo: normal and annulated gap junctions.

Neuroepithelial cells in the neural tube of 12 days old rat embryos make contact with each other by extended junctional complexes between their lateral membranes near the luminal surface. In this stage gap junctions are not numerous. Besides these "normal" gap junctions, especially in the upper part of the neuroepithelial cells, annulated gap junctions occur. They seem to originate by an endocytotic process of normal gap junctions with participation of cytoskeletal elements. The content of these annulated gap junctions mainly consists of ribosome-like particles in a high density, but larger particles may also occur. Annulated gap junctions sometimes reveal an intimate contact with the smooth endoplasmic reticulum or with the perinuclear cistern. If present in the perinuclear region the annulated gap junctions show membrane irregularities and other signs which are thought to mark steps of breakdown. Life-cycle and possible functions of the annulated gap junctions during neurulation need further investigation.

Animals↗

PubMed1988

Effects of colchicine- and cytochalasin B-treatment on the intracellular distribution of yolk droplets, lipid bodies, and Golgi apparatus of the chick neuroepithelial cells.

Treatment with colchicine (antimicrotubular agent) and cytochalasin B (antimicrofilamentous agent) has been used to investigate the possible role played by the cytoskeleton in the maintenance of intracellular distribution of yolk droplets, lipid bodies, and Golgi apparatus of the chick neuroepithelial cells. On the one hand, embryos treated with colchicine showed modifications in their distribution patterns of yolk droplets and lipid bodies, which suggests the involvement of the microtubular integrity of neuroepithelial cells in the maintenance of normal distribution patterns. On the other hand, the close relationships between vitelline and lipid inclusions and Golgi apparatus observed in untreated embryos seems to be kept in the embryos treated with colchicine and cytochalasin B. Moreover, from the effects of colchicine on Golgi apparatus position a possible functional role for the microtubular system in the maintenance of Golgi apparatus polarity in the chick neuroepithelial cells can be proposed. The results provided here constitute new information about the cellular mechanisms involved in chick neurulation.

Animals↗

PubMed2003

Ethanol blocks both basic fibroblast growth factor- and carbachol-mediated neuroepithelial cell expansion with differential effects on carbachol-activated signaling pathways.

We have expanded neuroepithelial cells dissociated from the embryonic rat telencephalon in serum-free defined medium containing basic fibroblast growth factor (bFGF) in order to generate a model neuroepithelium to study the interaction of ethanol with both growth factor- and transmitter-stimulated proliferation. Ethanol blocked proliferation stimulated by bFGF and by carbachol, an agonist at muscarinic acetylcholine receptors, in a dose-dependent manner. In addition, ethanol attenuated autonomous expansion of neuroepithelial cells occurring following withdrawal of bFGF. The latter effect was associated with an increase in the number of apoptotic cells identified by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling labeling. We studied the effects of ethanol on carbachol-stimulated signaling pathways critical to its proliferative effects. Ethanol significantly reduced carbachol-stimulated Ca(2+) signaling, as well as Erk1/Erk2, Akt and cyclic AMP-response element-binding phosphorylations in a dose-dependent manner. Comparison of the potency of ethanol in attenuating carbachol-stimulated proliferation and signal transduction showed that mitogen-activated protein kinase phosphorylation was less sensitive to ethanol than the other parameters. The results indicate that ethanol's suppression of proliferation induced by carbachol in this model neuroepithelium likely involves multiple signaling pathways. These effects in vitro may help to explain the devastating effects of prenatal ethanol exposure in vivo, which contribute to the fetal alcohol syndrome.

Acetylcholine↗

PubMed2003

Folic acid and homocysteine affect neural crest and neuroepithelial cell outgrowth and differentiation in vitro.

The beneficial effect of additional folic acid in the periconceptional period to prevent neural tube defects, orofacial clefts, and conotruncal heart defects in the offspring has been shown. Folate shortage results in homocysteine accumulation. Elevated levels of homocysteine have been related to neural tube defects. We studied the behavior of neuroepithelial cells and cranial and cardiac neural crest cells in vitro. Neural tube explants were cultured for 24 and 48 hr in medium after addition of folic acid and/or homocysteine. Folic acid addition increased neuroepithelial cell outgrowth and increased neural crest cell differentiation into nerve and smooth muscle cells. Addition of homocysteine increased neural crest cell outgrowth and migration from the neural tube and inhibited neural crest cell differentiation. Our findings suggest that neural tube defects caused by folate deficiency and hyperhomocysteinemia develop due to increased neuroepithelial to neural crest cell transformation. This increased transformation leads to a shortage of neuroepithelial cells in the neural tube. Defects in orofacial and conotruncal development are explained by abnormal differentiation of neural crest cells in the presence of high homocysteine concentrations. Our findings supports a critical role for folic acid and homocysteine in the development of neural tube defects and neural crest related heart malformations.

Animals↗