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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific antibodies against actin and tubulin have been used to follow the distribution and organization of actin and tubulin containing structures in N-18 neuroblastoma cells induced to sprout axons. Immunofluorescence microscopy shows that during the time of axonal sprouting microtubules converge into growing processes forming dense bundles in which individual microtubules cannot be resolved. In the growth cone where individual fluorescent fibers can again be distinguished microtubules seem to be excluded from the very margin. Actin is predominantly located at the cell periphery both in cell bodies and in cell processes. It appears to be present in areas of high surface motility and is especially abundant at the tip of the growth cone.
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PMID:Changes in intracellular organization of tubulin and actin in N-18 neuroblastoma cells during the process of axon extension induced by serum deprivation. 35 32

Monolayers of cultured neuroblastoma cells were examined for immunofluorescent reactivity with antibodies directed against actin, myosin or intermediate filaments. In well spread cells, antibody to intermediate filaments stained an intricate cytoplasmic network which extended as filament bundles into cell processes; in poorly spread or rounded cells, the antibody stained thick juxtanuclear filament bundles. By contrast, antibodies to actin or myosin reacted with microspikes and with axonal growth cones. The different topographical distribution of actin, myosin and intermediate filaments suggests that while actin and myosin may have roles in axon elongation, intermediate filaments may function as an internal cytoskeleton as well as in axoplasmic transport. The different distribution of intermediate filaments in well spread compared with rounded cells suggests that the cell makes its filaments prior to axon development and that the filaments subsequently unwind and migrate into the cell processes to form the axon skeleton.
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PMID:Immunofluorescence demonstrates the distribution of actin, myosin and intermediate filaments in cultured neuroblastoma cells. 39 54

Conjugates of horseradish peroxidase with the lectins ricin (d-galactose), wheat germ agglutinin (N-acetylglucosamine), phytohemagglutinin (N-acetylgalactosamine), and with cholera toxin (GM1 ganglioside) were used for a cytochemical detection of corresponding termin al carbohydrates, or glycolipids on cell surfaces of cultured neurons and neuroblastoma cells. Cells were labeled at 4 degrees C with the above ligands and their adsorptive endocytosis was studied after incubations at 37 degrees C in a medium free of ligand. Peroxidase was detected by the method of Graham and Karnovsky (J. Histochem. Cytochem. 14:291, 1966). Lectins and cholera toxin underwent endocytosis in cisternae and vesicles of GERL (Golgi-Endoplasmic Reticulum-Lysosome). We suggest that GERL is the primary ercipieint of adsorptively endocytosed plasma membrane "receptor"-ligand complexes which are thus degraded or possibly reutilized (recycling). Wheat germ agglutinin-horseradish peroxidase conjugates used in vivo for studies of retrograde axonal transport were significantly more sensitive than free horseradish peroxidase.
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PMID:The use of lectins and cholera toxin for the detection of surface carbohydrates of cultured neurons and neuroblastoma. 47 60

Changes in a posttranslational modification of tubulin, which accompany differentiation, have been studied in neuroblastoma-glioma hybrid cultured cells. The modification consists of the reversible enzymatic addition of a tyrosine to the COOH terminus of the alpha chain. Cytoplasmic tubulin purified from undifferentiated cells resembled that from adult mammalian brain in that half was in a form which can not accept tyrosine; of the remainder, which is a substrate for tubulin-tyrosine ligase, a higher proportion had COOH-terminal tyrosine. In the tubulin from differentiated cells, in which there had been extensive assembly of axonal microtubules from a preformed pool of subunits, the nonsubstrate tubulin was almost entirely replaced by the species with COOH-terminal tyrosine. In living cells, in the absence of protein synthesis, there was fixation of labeled tyrosine into cytoplasmic alpha chains which was extensive enough to be consistent with turnover, during the course of an hour, of the pre-existing COOH-terminal tyrosine. The alpha chain in the particulate fraction of the cells was comparably labeled, along with some unidentified low molecular weight components.
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PMID:Tubulin tyrosylation in vivo and changes accompanying differentiation of cultured neuroblastoma-glioma hybrid cells. 50 Jun 54

The current status of the published work on the lipid composition of isolated brain cells is reviewed and some new work on the sphingolipids of these cells is presented. In spite of considerable differences in isolation techniques between different groups, the lipid analyses of different cell preparations are similar enough to permit several generalizations. This fact is an encouraging sign that cell separation methods have considerable usefulness in defining the composition of normal brain cells. It is a general finding that astrocytes have more lipid than neuronal perikarya but that the gross lipid composition of these two cell types is surprisingly similar. Oligodendroglial lipids are quite different from those of the other two cell types and are characterized by a high galactolipid content. Although such a lipid pattern might be expected in oligodendroglia, which are myelin-forming cells, axonal lipids have an even higher galactolipid content. In an effort to find more cell-specific patterns, the glycosphingolipids were examined in more detail. Differences were seen in the distribution and fatty-acid patterns of these minor lipids in neurons and astrocytes, although it may be premature to conclude that these differences will prove to be cell-specific. All of the isolated cells were found to contain galactosylceramide, sulfatide, glucosylceramide, dihexosylceramide, and gangliosides. The distribution of these lipids in the normal cells was found to differ considerably from that reported in cultured neuroblastoma cells or astrocytoma cells. Not only were gangliosides present in all cells but the ganglioside patterns of neurons and astrocytes were nearly identical. The fatty-acid patterns of the neuronal and astroglial sphingolipids generally do not resemble each other, and both are quite different from those found in oligodendroglia and axons. However, the fatty-acid composition of the sphingolipids from bovine oligodendroglia and from axons are similar and resemble those of myelin lipids. The fatty acids of glucosylceramide and dihexosylceramide are similar in all three cell types. They have rather large amounts of 16:0 and acids longer than C18; thus they are considerably different from the ganglioside fatty acids (which have mostly 15:0) isolated from the same fractions.
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PMID:The lipid composition of isolated brain cells and axons. 122 19

N1E.115 murine neuroblastoma cells differentiating in serum-free medium were used to develop a paradigm for testing neurotoxicity in vitro. The paradigm was designed to test the effects of toxicants on four different aspects of cell function or structure: 1. Viability as shown by the retention of cellular radiolabel (51Cr); 2. Growth and maintenance of neurites as reflected by the incidence and average length of these processes; 3. Gross structure of neurites; and 4. Velocity and flux of rapid anterograde and retrograde axonal transport as judged by video-enhanced differential interference contrast microscopy. To evaluate this paradigm, colchicine and vinblastine were used as neurotoxicants with a well-understood mechanism of action. These agents were only weakly cytotoxic according to the Cr-release assay, but were able to interfere with neurite outgrowth at nanomolar concentrations. Neurites that were elaborated in the presence of vinblastine and colchicine were often disfigured by numerous swellings packed with organelles. In established neurites, micromolar concentrations of vinblastine inhibited organellar motility with great rapidity, blocking all signs of transport within 20 min. The effect of colchicine was slower and less complete, but still impressive. We suggest that this four-part analysis represents a highly sensitive in vitro test for neurotoxicity, and a means of analyzing the relation between abnormalities of transport and structural damage of nerve cells.
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PMID:A paradigm for examining toxicant effects on viability, structure, and axonal transport of neurons in culture. 128 27

Morphological rearrangements, such as synapse number changes, have been observed in the adult mammalian brain after various experimental paradigms of learning and behavioral experience. The role of axonal transport in the physical translocation of material during this form of brain plasticity has not been fully appreciated. We show here by quantitative video microscopy that sabeluzole (R58735), a new memory-enhancing drug in humans, effectively increases fast axonal transport in rat neuronal cell cultures. Long-term incubation (24 hr) with sabeluzole in the concentration range between 0.1 and 1 microM increases both velocity and jump length of saltatory movements maximally by 20-30% in embryonic hippocampal neurons. Acute treatment only increases the velocity by 15-20%. Furthermore, the inhibition of axonal transport by 0.1 mM vanadate in N4 neuroblastoma cells is reversed by 1 microM sabeluzole. Observations on the kinesin-induced microtubule mobility in a reconstituted system show a 10% enhancement by sabeluzole at an optimal concentration of 2 microM, but no increase in kinesin ATPase activity. To our knowledge, this is the first pharmacological compound shown to increase fast axonal transport. The mechanism of fast axonal transport enhancement is discussed as a rationale for new therapeutic treatment in neuropathology.
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PMID:Sabeluzole, a memory-enhancing molecule, increases fast axonal transport in neuronal cell cultures. 137 35

NB2a/d1 neuroblastoma cells constitutively express multiple isoforms of the microtubule-associated protein tau and incorporate this protein into the axonal neurites elaborated during serum deprivation. To examine whether or not tau played an essential role in axonal outgrowth, cells cultured in serum-free medium were treated at 24 h intervals with antisense- and sense-oriented cDNA oligonucleotides (25 or 36 mers that span or are upstream of tau initiation codon) and were simultaneously serum deprived. Oligonucleotide uptake was confirmed by determination of intracellular levels of radiolabeled oligonucleotides. Treatment for 48 h with tau antisense oligonucleotides reversibly inhibited the expression of tau and the number of neurite-bearing cells compared with treatment with sense oligonucleotides. By contrast, tubulin expression was not affected. When cells were treated with antisense oligonucleotide simultaneously with serum deprivation, the initial outgrowth of neurites was unaffected, but continued neurite elongation was prevented. By contrast, neurite outgrowth at 4 h was inhibited when cells were pretreated with tau antisense 24 h before serum deprivation. Furthermore, intracellular delivery of anti-tau antiserum prevented neurite outgrowth and, in cells that had previously been deprived of serum for 24 h, induced retraction of existing neurites. These findings indicate that both the initiation and the continued outgrowth of neurites are dependent on tau and that pre-existing cytoplasmic pools of tau can mediate initial neuritogenesis.
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PMID:Microtubule-associated protein tau is required for axonal neurite elaboration by neuroblastoma cells. 143 85

The precise regional control of cell adhesion and growth on a substrate may create two-dimensional tissue formation, as in a neural network. To prepare a neural circuit, micropositioning of neural cells and guidance of extending axons in a given region are required. In general, the adhesion of neural cells and their axonal extension are mediated by adhesive proteins found in the extracellular matrix. This paper describes a novel surface photoprocessing that enables the creation and guidance of regionally selective cell adhesion, leading to a neural network. The non-adherent region was created by chemical fixation of a photoreactive hydrophilic co-polymer of azidostyrene and N, N-dimethylacrylamide on a hydrophobic substrate. Ultraviolet irradiation with the use of a photomask placed on a substrate hydrophilically modified the irradiated regions, which was evident in ESCA and contact angle measurements. The addition of a collagen buffer solution resulted in collagen adsorption only on the non-irradiated hydrophobic portions. Seeded neuroblastoma cells adhered only on collagen-adsorbed pathways 130 microns in width. One day after seeding, nerve growth factor was added to the culture medium, resulting in cell differentiation from growth to axonal extension. The axons grew along the collagen-adsorbed pathways. Sooner or later, cells were interconnected with extended axons, which was clearly visible microscopically. Further culturing completed the honeycomb-like patterning, as designed. The surface processing developed here can manipulate fundamental cellular behavior, leading to two-dimensional patterned tissue, which may provide information on the morphogenesis of the neural network and neurotransmission.
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PMID:Two-dimensional cell manipulation technology. An artificial neural circuit based on surface microphotoprocessing. 145 57

Increased titers of anti-sulfatide antibodies were detected by ELISA in 5 of 200 patients and control subjects. All 5 patients had sensory impairment; 4 had neuropathy, and one had multiple sclerosis. Of the patients with neuropathy, 2 had a clinical syndrome of small fiber sensory neuropathy with normal electrophysiological or nerve biopsy studies, 1 had a sensorimotor axonal neuropathy associated with IgM monoclonal gammopathy, and 1 had sensorimotor neuropathy with multifocal motor conduction block and anti-GM1 antibodies. The anti-sulfatide antibodies bound to the surface of unfixed rat dorsal root ganglia neurons and human neuroblastoma cells, and to fixed sections of central and peripheral myelin. No binding was detected following intraneural injection into rat sciatic nerves. Pre-absorption with sulfatide but not with galactocerebroside eliminated the tissue binding activity. These findings indicate that increased titers of anti-sulfatide antibodies are found in patients with sensory impairment but are not restricted to a particular neurological syndrome or type of neuropathy. The significance of anti-sulfatide antibodies is uncertain although sulfatide on dorsal root ganglia neurons may be a target antigen.
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PMID:Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons. 146 27


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