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PubMed1996

Roles of cell-autonomous mechanisms for differential expression of region-specific transcription factors in neuroepithelial cells.

Although a number of genes have been found to have restricted expression domains in the embryonic forebrain and midbrain, it remains largely unknown how the expression of these genes is regulated at the cellular level. In this study, we explored the mechanisms for the differential expression of region-specific transcription factors in neuroepithelial cells by using both primary and immortalized neuroepithelial cells from the rat brain at embryonic day 11.5. We found that differential expression patterns of Pax-3, Pax-5, Pax-6, Dlx-1, Dlx-2, Emx2, Otx1 and Dbx observed in vivo were maintained even when the cells were isolated and cultured in vitro, free from environmental influences. Furthermore, in response to Sonic hedgehog, which is a major inductive signal from the environment for regional specification, neuroepithelial cells that maintain distinct regional identities expressed different sets of ventral-specific genes including Islet-1, Nkx-2.1 and Nkx-2.2. These results suggest that certain cell-autonomous mechanisms play important roles in regulating both environmental signal-dependent and -independent expression of region-specific genes. Thus, we propose that use of the in vitro culture systems we describe in this study facilitates the understanding of regulatory mechanisms of region-specific genes in neuroepithelial cells.

Animals↗
PubMed1994

Heterogeneity among neuroepithelial cells in the chick retina revealed by immunostaining with monoclonal antibody PM1.

Neuroepithelial cells appear as a homogeneous population of cells in the cell cycle that seem to behave as pluripotent neural precursors. The study of the intrinsic heterogeneity and subtle developmental changes among neuroepithelial cells has been hindered by the lack of specific markers. To address that study, a panel of monoclonal antibodies was produced against early developing chick retina. The monoclonal antibody precursor marker 1 (PM1) labels most, if not all, of the early neuroepithelial cells in embryonic day 4 retinal sections. This pattern is transient since the labelling becomes restricted to the peripheral retina as development proceeds and eventually disappears from the neuroepithelial cells. However, apparently in parallel, the differentiating retinal ganglion cells become PM1-positive. The expression of the PM1 antigen, a 73 x 10(3) M(r) protein, as shown by western blotting, also decreases with development. In addition, a chick retina dissociated-cell culture system, where retinal neuroepithelial cells actively proliferate and undergo differentiation under defined conditions, in combination with monoclonal antibody PM1, allowed us to characterize and quantify the proliferating and differentiating neuroepithelial cells. Interestingly, the fraction of total neuroepithelial cells that are stained with PM1 sharply decreases as retinal development proceeds, in correlation with the staining pattern in sections from matched stages. These data thus reveal that the pluripotent neural precursors in the chick retina already represent an intrinsically heterogeneous population, and that this population changes with development.

Animals↗
PubMed2004

Asymmetric distribution of the apical plasma membrane during neurogenic divisions of mammalian neuroepithelial cells.

At the onset of neurogenesis in the mammalian central nervous system, neuroepithelial cells switch from symmetric, proliferative to asymmetric, neurogenic divisions. In analogy to the asymmetric division of Drosophila neuroblasts, this switch of mammalian neuroepithelial cells is thought to involve a change in cleavage plane orientation from perpendicular (vertical cleavage) to parallel (horizontal cleavage) relative to the apical surface of the neuroepithelium. Here, we report, using TIS21-GFP knock-in mouse embryos to identify neurogenic neuroepithelial cells, that at the onset as well as advanced stages of neurogenesis the vast majority of neurogenic divisions, like proliferative divisions, show vertical cleavage planes. Remarkably, however, neurogenic divisions of neuroepithelial cells, but not proliferative ones, involve an asymmetric distribution to the daughter cells of the apical plasma membrane, which constitutes only a minute fraction (1-2%) of the entire neuroepithelial cell plasma membrane. Our results support a novel concept for the cell biological basis of asymmetric, neurogenic divisions of neuroepithelial cells in the mammalian central nervous system.

Animals↗
PubMed1998

In vitro-model for Toxoplasma gondii invasion into neuroepithelial cells.

In order to study the interactions of Toxoplasma gondii and neuroepithelial cells morphologically and biochemically we established an easy in vitro model, which simulates cellular contacts in congenital toxoplasmosis. Monolayer cultures of neuroepithelial cells from 13-14-day-old mouse embryos were prepared containing the typical ventricular cell types found in an embryonic brain, such as young neurons, macroglial and microglial cells. Ultrastructural investigations on cultures incubated for 1, 5 and 30 min or 1, 6, 12, 24 and 48 h with T. gondii indicated that all three cell types had been invaded by the parasites, multiplying in parasite vacuoles by means of endodyogeny. Microglial cells had already been penetrated by trophozoites within one minute and showed up to 3 or 5 parasite vacuoles per cell. Neurons and glial cells were invaded within 5 min and contained only one vacuole per host cell. All the parasite vacuoles were bounded by a membrane and bordered by the rough endoplasmic reticulum and mitochondria of the host cell after a few minutes. The vacuoles also contained some membranic tubuli. After 30 min some neuronal neurites were destroyed while the perikarya seemed to be unchanged. After 6 h the cytoplasm of the microglia lost more and more ribosomes and organelles. Neurons and glial cells showed no alterations. After 12h large areas of the vacuole membrane were folded up and lay curled up in the vacuoles. After 24 h incubation T. gondii had destroyed nearly all the microglial cells. The ultrastructure of neurons and glial cells now began to change in the same way as shown for microglial cells. The organelles and cellular membranes disintegrated and after 48 h incubation nearly all the cells in the neuroepithelial cell culture had fallen to pieces. For an identification of T. gondii in vitro by light microscopy or for the characterization of the cell surface we tried to label the parasites with 11 different FITC-stained lectins. None of the tested lectins bound to the parasites. We conclude that our in vitro-model for invasion of T. gondii in neuroepithelial cells opens an opportunity for studying the interaction of these cells or the pharmacological effects on this interaction under defined conditions.

Animals↗
PubMed1992

The neuroepithelial cells of the fish gill filament: indolamine-immunocytochemistry and innervation.

The neuroepithelial cells (NECs) of the fish gill filament share several morphofunctional features with the cells of the neuroepithelial bodies in the lungs of air-breathing vertebrates. In the present study, a detailed indolamine-immunocytochemical analysis of the branchial neuroepithelial cells and nerves was undertaken in non-teleost and teleost species, with particular emphasis on the latter. In the rainbow trout, Oncorhynchus mykiss, the chemical degeneration of either catecholaminergic (by 5- and 6-hydroxydopamines) or indolaminergic (by 5,6-dihydroxy-tryptamine) innervations associated with the NECs was studied using electron microscopy. In teleosts, the NECs are located primarily on the distal half of the filament. In the trout particularly, these cells are innervated mainly by non-indolaminergic nerves taking up sympathetic neurotoxins. The proximal half of the filament contains isolated NECs innervated additionally by intrinsic indolaminergic neurons. Serotonin-like immunoreactivity of the NECs is evident in the granular vesicles packed within the basal soma and processes which surround non-vascular and vascular smooth muscles in the filament. Apical processes from the neuroepithelial cells occasionally contact the water on the surface of the filament epithelium. The secretory function of the NECs is discussed with reference to the probable involvement of serotonin in the modulation of fish gill function. In addition, their connections with both central and branchial nervous systems suggest a possible chemoreceptor role.

Animals↗
PubMed1994

Quantitative analyses of neuroepithelial cell shapes during bending of the mouse neural plate.

Despite a wealth of information about cell behaviors contributing to neurulation in chick embryos, similar behaviors in mouse embryos have yet to be well characterized. This study examines cell behaviors occurring during bending of the mouse neural plate, in particular, qualitative and quantitative changes in neuroepithelial cell shape. Our current results demonstrate that in mouse embryos 1) the median hinge point (MHP), a localized region of neural plate that becomes anchored to the underlying prechordal plate mesoderm or notochord/notochordal plate and forms a midline longitudinal furrow around which folding of the remaining neural plate (i.e., the part of the neural plate not involved in MHP formation) occurs, develops during stages of neural fold elevation; 2) the MHP is enriched with wedge-shaped neuroepithelial cells but has significantly fewer spindle-shaped, inverted wedge-shaped, and globular neuroepithelial cells than do the adjacent paired lateral areas of the neuroepithelium (L); and 3) each L is enriched with spindle-shaped, inverted wedge-shaped, and globular neuroepithelial cells but has significantly fewer wedge-shaped neuroepithelial cells than does the MHP. Thus wedging of neuroepithelial cells occurs during bending of the mouse neural plate and is localized to the MHP during neural fold elevation. Similarly, previous studies in the chick have shown that neuroepithelial cells become wedge shaped during bending of the neural plate and that such cell wedging is localized to the MHP during neural fold elevation. Such studies also have shed light on the roles of MHP formation and localized wedging of neuroepithelial cells within the MHP in the chick; however, such roles have yet to be elucidated in the mouse.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Rod photoreceptor development in vitro: intrinsic properties of proliferating neuroepithelial cells change as development proceeds in the rat retina.

We describe a reaggregated cell culture system in which retinal neuroepithelial cells from embryonic rats proliferate extensively and give rise to rod photoreceptors on the same schedule in vitro as they do in vivo. Both the proliferative potential of the embryonic neuroepithelial cells and the timing of their differentiation into rods are not changed by the presence of a 50-fold excess of neonatal neural retinal cells, although many more of the embryonic cells develop into rods in these circumstances. In such mixed-age cultures, dividing neonatal cells proliferate much less and give rise to rods much sooner than do dividing embryonic cells, suggesting that the dividing cells at the two ages are intrinsically different. These and other findings suggest that both cell-cell interactions and an intrinsic program in neuroepithelial cells determine cell fate in the developing rat retina.

Aging↗
PubMed1991

Basic fibroblast growth factor upregulates steady-state levels of laminin B1 and B2 chain mRNA in cultured neuroepithelial cells.

The growth of purified populations of murine neuroepithelial cells isolated from 10 day embryonic (E10) telencephalon and mesencephalon can be specifically enhanced by supplementing growth culture media with basic fibroblast growth factor (bFGF). One effect of bFGF on cultured neuroepithelial cells was to enhance the amount of laminin expressed at the protein level as detected by immunofluorescence. This was correlated with significant upregulation of steady-state levels of laminin B1 and B2 chain expression as analyzed at the mRNA level. When E12 neuroepithelial cells were split into precursor neuronal or glial subpopulations on the basis of differential expression of major histocompatibility class-1 antigens, only the glial progenitor fraction was found to be capable of detectable laminin synthesis. It is thus possible that a primary action of FGF is to increase the synthesis and release of extracellular matrix molecules from neural cells which act back in a paracrine manner to stimulate differentiation.

Animals↗
PubMed2003

A dual role for Sonic hedgehog in regulating adhesion and differentiation of neuroepithelial cells.

In vertebrates, the nervous system arises from a flat sheet of epithelial cells, the neural plate, that gradually transforms into a hollow neural tube. This process, called neurulation, involves sequential changes in cellular interactions that are precisely coordinated both spatially and temporally by the combined actions of morphogens. To gain further insight into the molecular events regulating cell adhesion during neurulation, we investigated whether the adhesive and migratory capacities of neuroepithelial cells might be modulated by Sonic hedgehog (Shh), a signaling molecule involved in the control of cell differentiation in the ventral neural tube. When deposited onto extracellular matrix components in vitro, neural plates explanted from avian embryos at early neurulation readily dispersed into monolayers of spread cells, thereby revealing their intrinsic ability to migrate. In the presence of Shh added in solution to the culture medium, the explants still exhibited the same propensity to disperse. In contrast, when Shh was immobilized to the substrate or produced by neuroepithelial cells themselves after transfection, neural plate explants failed to disperse and instead formed compact structures. Changes in the adhesive capacities of neuroepithelial cells caused by Shh could be accounted for by inactivation of surface beta1-integrins combined with an increase in N-cadherin-mediated cell adhesion. Furthermore, immobilized Shh promoted differentiation of neuroepithelial cells into motor neurons and floor plate cells with the same potency as soluble Shh. However, the effect of Shh on the neuroepithelial cell adhesion was discernible and apparently independent from its differentiation effect and was not mediated by the signaling cascade elicited by the Patched-Smoothened receptor and involving the Gli transcription factors. Thus, our experiments indicate that Shh is able to control sequentially adhesion and differentiation of neuroepithelial cells through different mechanisms, leading to a coordinated regulation of the various cell interactions essential for neural tube morphogenesis.

Animals↗
PubMed1983

Anomalies of neuroepithelial cell associations in the Splotch mutant embryo.

Neuroepithelial development in Splotch mutant mouse embryos was examined using SEM and TEM. Unlike unaffected littermates, Sp/Sp embryos exhibited extensive neural tube closure defects, disorganization and misalignment of neuroepithelial cells in regions with open defects. Neuroepithelial cell processes often made lateral progress in these areas rather than maintaining their normal contact with the luminal surface. In addition, intercellular space was considerably increased and there were many ectopic cell processes in basal regions of affected areas. The role of altered cell-cell interactions in neurulation is considered.

Animals↗
PubMed1989

Organelle distribution in chick neuroepithelial cells: effects of colchicine and cytochalasin B.

The intracellular distribution of mitochondria, cytoplasmic inclusions and rough endoplasmic reticulum cisternae of chick neuroepithelial cells was investigated at neurulation stages 6, 8, 10 and 12. These neuroepithelial cells were subdivided into three zones: apical, median and basal and the distribution percentages of distribution of these organelles were obtained. Mitochondrial distribution was related to the energy supply that mitochondria provide for apical microfilament contraction. Cytoplasmic inclusions were distributed preferentially in the apical zone of the neuroepithelial cells during the four stages. Rough endoplasmic reticulum cisternae were homogeneously distributed in the three zones at stages 10 and 12, but at stages 6 and 8 there are more elevated percentages of rough endoplasmic reticulum in the apical zones than in the other zones. Experimental treatments with colchicine and cytochalasin B does not modify the patterns of mitochondria and rough endoplasmic reticulum cisternae but alters the distribution of cytoplasmic inclusions. Finally, there is a correlation in the normal neurulating neuroepithelial cells between the distributions of mitochondria and rough endoplasmic reticulum distribution and between the distributions of mitochondria and cytoplasmic inclusions distribution. This relationship is retained in the treated neuroepithelial cells.

Animals↗
PubMed1982

Neuroepithelial cells in fish gill primary lamellae.

Formaldehyde-induced fluorescence reveals numerous serotonin-containing cells within the primary epithelium of the fish gill. These cells are isolated or clustered and are supported by the epithelial basal lamina. They never reach the external medium and are found on the internal side of the primary lamellae, facing the respiratory water flow. With the electron microscope, these cells are found to contain dense-cored vesicles (DCV) of 80-100 nm. Nerve profiles are consistently found close to DCV cells. After having crossed the basal lamina, nerve fibers form endings on DCV-containing cells. These endings display both small clear vesicles and DCV and are in direct contact with DCV cells. Specific membrane alterations are suggestive of efferent synapses. These cells are considered neuroepithelial cells, similar to those found within the wall of lung airways in mammals and submammalian vertebrates. Structure and localization are suggestive of a tissue O2 sensor.

Animals↗
PubMed1992

Neuroepithelial cells in the rat spinal cord express glutamate decarboxylase immunoreactivity in vivo and in vitro.

It is unknown whether neuroepithelial cells in the mammalian central nervous system express neurotransmitter-synthesizing enzymes. In this study, expression of glutamate decarboxylase (GAD), the gamma-aminobutyric acid (GABA)-synthesizing enzyme, was examined in proliferative cells and postmitotic neuroblasts in embryonic rat spinal cord. Immunostaining coronal sections of the embryonic spinal cord with K2 antiserum, which recognizes GAD proteins encoded by the GAD67 gene, revealed intensely stained neuroepithelial cells in the basal plate at embryonic day (E) 13, in the intermediate plate between E 13-16, and last seen in the alar plate at E 16. Nissl counterstaining demonstrated that a small number of these GAD-immunoreactive cells adjacent to the neural tube lumen were mitotic. The ventral-to-dorsal gradient of GAD expression in precursor cells and postmitotic neuroblasts correlates anatomically and temporally with the sequential generation of motoneurons, commissural neurons, and interneurons in the dorsal horn. Some of these GAD-immunoreactive neuroepithelial cells may re-enter the mitotic cycle, while others are postmitotic neuroblasts presumably migrating to the intermediate zone to differentiate into young neurons. Double-immunostaining cells acutely dissociated from E 11-18 spinal cords with K2 and anti-bromodeoxyuridine antisera, following a bromodeoxyuridine pulse in vivo, revealed considerable numbers of DNA-synthesizing cells immunoreactive for GAD. The absolute number of double-stained cells peaked during E 12-15, coinciding with terminal cell division in most spinal neurons. These observations suggest that spinal neuronal precursors can synthesize GAD-related proteins prior to, or during, the terminal cell cycle. Although GAD immunoreactivity revealed by K2 antiserum was detected in proliferative cells and in migrating postmitotic neuroblasts, GABA immunoreactivity was never detectable in these cells. These early embryonic GAD-immunoreactive neuroepithelial cells may either synthesize levels of GABA that cannot be detected immunocytochemically, and/or express enzymatically inactive GAD-related proteins.

Animals↗
PubMed2006

Inactivation of aPKClambda results in the loss of adherens junctions in neuroepithelial cells without affecting neurogenesis in mouse neocortex.

In developing mammalian telencephalon, the loss of adherens junctions and cell cycle exit represent crucial steps in the differentiation of neuroepithelial cells into neurons, but the relationship between these cellular events remains obscure. Atypical protein kinase C (aPKC) is known to contribute to junction formation in epithelial cells and to cell fate determination for Drosophila neuroblasts. To elucidate the functions of aPKClambda, one out of two aPKC members, in mouse neocortical neurogenesis, a Nestin-Cre mediated conditional gene targeting system was employed. In conditional aPKClambda knockout mice, neuroepithelial cells of the neocortical region lost aPKClambda protein at embryonic day 15 and demonstrated a loss of adherens junctions, retraction of apical processes and impaired interkinetic nuclear migration that resulted in disordered neuroepithelial tissue architecture. These results are evidence that aPKClambda is indispensable for the maintenance of adherens junctions and may function in the regulation of adherens junction integrity upon differentiation of neuroepithelial cells into neurons. In spite of the loss of adherens junctions in the neuroepithelium of conditional aPKClambda knockout mice, neurons were produced at a normal rate. Therefore, we concluded that, at least in the later stages of neurogenesis, regulation of cell cycle exit is independent of adherens junctions.

Adherens Junctions↗
PubMed1988

Organelle distribution in the wedge-, spindle- and inverted wedge-shaped neuroepithelial cells during chick embryo neurulation.

The formation of the neural tube is a morphogenetic process involving cell-shape changes. The activity of the cytoskeletal elements of the neuroepithelial cells and the interkinetic nuclear migration affect the neuroepithelial cell shape in a way that these cells acquire three distinct conformations of wedge-shaped, spindle-shaped and inverted wedge-shaped cells. Each of them is ultrastructurally characterized in this paper with regard to the intracellular distribution of mitochondria, rough endoplasmic reticulum, yolk droplets, lipid bodies and Golgi apparatus. These distribution patterns are analyzed in relation to the role played by the neuroepithelial cells during the successive phases of neural tube formation.

Animals↗
PubMed2005

Cell cycle inhibition by sodium arsenite in primary embryonic rat midbrain neuroepithelial cells.

Arsenite (As3+) exposure during development has been associated with neural tube defects and other structural malformations, and with behavioral alterations including altered locomotor activity and operant learning. The molecular mechanisms underlying these effects are uncertain. Because arsenic can cross the placenta and accumulate in the developing neuroepithelium, we examined cell cycling effects of sodium arsenite (As3+ 0, 0.5, 1, 2, and 4 microM) on embryonic primary rat midbrain (gestational day [GD] 12) neuroepithelial cells over 48 h. There was a concentration- and time-dependent As3+-induced reduction in cell viability assessed by neutral red dye uptake assay but minimal apoptosis at concentrations below 4 microM. Morphologically, apoptosis was not apparent until 4 microM at 24 h, which was demonstrated by a marginal but statistically significant increase in cleaved caspase-3/7 activity. Cell cycling effects over several rounds of replication were determined by continuous 5-bromo-2'-deoxyuridine (BrdU) labeling and bivariate flow cytometric Hoechst-Propidium Iodide analysis. We observed a time- and concentration-dependent inhibition of cell cycle progression as early as 12 h after exposure (> or =0.5 microM). In addition, data demonstrated a concentration-dependent increase in cytostasis within all cell cycle phases, a decreased proportion of cells able to reach the second cell cycle, and a reduced cell cycle entry from gap 1 phase (G1). The proportion of affected cells and the severity of the cell cycle perturbation, which ranged from a decreased transition probability to complete cytostasis in all cell cycle phases, were also found to be concentration-dependent. Together, these data support a role for perturbed cell cycle progression in As3+ mediated neurodevelopmental toxicity.

Animals↗
PubMed1997

Glial-restricted precursors are derived from multipotent neuroepithelial stem cells.

Neuroepithelial cells in the developing ventricular zone differentiate into neurons, astrocytes, and oligodendrocytes. It is not known, however, whether this differentiation occurs in a single step or is a pathway utilizing intermediate more restricted precursor cells. To characterize the generation of glial cells from multipotent stem cells we have cultured neuroepithelial (NEP) cells from E10.5 rat embryos. Cultured NEP cells do not express any glial differentiation markers when grown on fibronectin/laminin under nondifferentiation conditions. NEP cells, however, differentiate into A2B5 immunoreactive cells which can subsequently give rise to oligodendrocytes and astrocytes. Clonal analysis of NEP cells demonstrates that the A2B5 immunoreactive cells arise in clones that contain neurons and astrocytes, indicating that A2B5(+) cells arise from multipotent NEP precursor cells. A2B5(+) cells, maintained as undifferentiated cells over multiple passages, can subsequently give rise to both oligodendrocytes and astrocytes. A2B5(+) cells, however, do not generate neurons. Thus A2B5(+) cells represent a restricted progenitor cell population that differentiates from a multipotent NEP cell. Based on our results we propose that differentiation of the multipotential NEP cells to terminally differentiated glial cells occurs via intermediate restricted precursors.

Animals↗