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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Recent experiments on the development of neural segmentation in chick embryos are reviewed. 2. Segmentation of the spinal peripheral nerves is governed by a subdivision of the somite-derived sclerotome into anterior and posterior halves. Migrating neural crest cells and outgrowing motor axons are confined to the anterior sclerotome as a result, in part, of inhibitory interactions with posterior sclerotome cells. 3. The sclerotomal distribution of certain molecules known to influence growing nerve cells in vitro, namely laminin, fibronectin, N-CAM, N-Cadherin and J1/tenascin/cytotactin, suggest that these molecules play no critical role in determining the preference of nerve cells for anterior sclerotome. 4. Peanut agglutinin (PNA) recognises cell surface-associated components on posterior cells which, when incorporated into liposomes, cause the abrupt collapse of sensory growth cones in vitro. The PNA receptor(s) may be inhibitory for nerve cells in vivo. 5. The chick hindbrain epithelium is segmented early in its development. Each branchiomotor nucleus in the series of cranial nerves V, VII and IX derives from a pair of segments lying in register with an adjacent branchial arch. Neurogenesis of motor and reticular axons begins in alternate segments, suggesting parallels with insect pattern formation.
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PMID:Segmentation and the development of the vertebrate nervous system. 219 47

Janusin and tenascin are glia-derived, structurally related, extracellular matrix glycoproteins of the J1 family that are expressed in vivo at times and in locations where active neurite outgrowth occurs, but also when the formation or stabilization of cytoarchitectonic boundaries appears to be in operation. To resolve this apparent functional dichotomy, we have studied the behavioral response of growth cones, growing in culture on the permissive substrate laminin to janusin and tenascin, by video time lapse microscopy. When janusin and tenascin were offered as sharp substrate boundaries, dorsal root ganglion (DRG) and retinal ganglion neuron growth cones avoided growing on these molecules, but were not induced to collapse. On the other hand, when janusin and tenascin were offered, in a mixture with laminin, as uniform substrates, DRG growth cones displayed a collapsed morphology and were able to advance at a faster rate than on laminin alone. In contrast, the outgrowth of retinal ganglion neuron growth cones was completely inhibited under these conditions, underscoring a cell type specificity in the response of growth cones to these molecules. Using several monoclonal antibodies binding to distinct epitopes on the tenascin molecule, we have identified two domains responsible for growth cone repulsion, on epidermal growth factor (EGF)-like repeats 3-5 and fibronectin type III homologous repeats 4 and 5. These domains are different from the one previously recognized to be involved in neurite outgrowth on a uniform tenascin substrate. We conclude that both molecules may promote or retard growth cone advance, depending on the spatial expression pattern and the neuronal cell type.
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PMID:Influence of janusin and tenascin on growth cone behavior in vitro. 768 56

Axon growth-promoting and -inhibitory molecules are likely to work in concert to promote and guide axons in vivo. In adult mammals, inhibitory molecules associated with myelin in the white matter of the central nervous system (CNS) play an important role in the failure of long-distance axon regeneration. The presence of neurite growth-inhibitory molecules in the adult rat gray matter has not been extensively studied. In this article we describe work on the characterization of neurite growth-inhibitory activity in the adult rat cerebral cortical gray matter using various biochemical and cell culture approaches. We show using a neuronal cell line (NG108-15 cells) that neurite growth-inhibitory activity is present in membrane preparations of the cortical gray matter. Purified gray matter membranes also induce growth cone collapse of cultured embryonic rat dorsal root ganglion neurons. The inhibitory activity in the membrane preparations is extractable with 3-[(3-cholamidoprophyl)-dimethylammonio]-1-propane-sulfonate, but does not appear to be depleted by various lectins. Western blots and enzyme treatments showed that the inhibitory effect of the gray-matter preparations is not likely to be mediated by myelin-associated inhibitors or chondroitin sulfate proteoglycans. However, tenascin was detected in these samples and may contribute to some of the inhibitory activity. Selective separation of the inhibitory molecules can be achieved by ion-exchange chromatography, which also suggests the presence of multiple inhibitors in cortical gray matter membranes.
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PMID:Neurite growth-inhibitory activity in the adult rat cerebral cortical gray matter. 918 45

Several molecules have been identified as potential sources of the barriers to glial cell mixing and sensory regeneration that exist at the boundary between the peripheral and central nervous systems, including tenascin-C, tenascin-R, chondroitin sulfate proteoglycans, and NG2. Here we show that tenascin-Y, the avian homologue of tenascin-X, is concentrated in the proximal portions of peripheral nerves in the chicken. In vitro analyses of cultures enriched for Schwann cells demonstrate that recombinant tenascin-Y has dose-dependent effects on glial cell attachment, spreading, and migration. In addition, nanomolar concentrations of tenascin-Y cause the rapid collapse of sensory growth cones cultured on fibronectin, and regenerating sensory neurites preferentially migrate on fibronectin and avoid tenascin-Y in microstripe assays. We conclude that the expression pattern of tenascin-Y and its properties in vitro are consistent with a role as an inhibitor of glial cell migration and sensory regeneration in nerve roots.
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PMID:Tenascin-Y is concentrated in adult nerve roots and has barrier properties in vitro. 1174 61

Axon regeneration is arrested in the injured central nervous system (CNS) by axon growth-inhibitory ligands expressed in oligodendrocytes/myelin, NG2-glia, and reactive astrocytes in the lesion and degenerating tracts, and by fibroblasts in scar tissue. Growth cone receptors (Rc) bind inhibitory ligands, activating a Rho-family GTPase intracellular signaling pathway that disrupts the actin cytoskeleton inducing growth cone collapse/repulsion. The known inhibitory ligands include the chondroitin sulfate proteoglycans (CSPG) Neurocan, Brevican, Phosphacan, Tenascin, and NG2, as either membrane-bound or secreted molecules; Ephrins expressed on astrocyte/fibroblast membranes; the myelin/oligodendrocyte-derived growth inhibitors Nogo, MAG, and OMgp; and membrane-bound semaphorins (Sema) produced by meningeal fibroblasts invading the scar. No definitive CSPG Rc have been identified, although intracellular signaling through the Rho family of G-proteins is probably common to all the inhibitory ligands. Ephrins bind to signalling Ephs. The ligand-binding Rc for all the myelin inhibitors is NgR and requires p75(NTR) for transmembrane signaling. The neuropilin (NP)/plexin (Plex) Rc complex binds Sema. Strategies for promoting axon growth after CNS injury are thwarted by the plethora of inhibitory ligands and the ligand promiscuity of some of their Rc. There is also paradoxical reciprocal expression of many of the inhibitory ligands/Rc in normal and damaged neurons, and NgR expression is restricted to a limited number of neuronal populations. All these factors, together with an incomplete understanding of the normal functions of many of these molecules in the intact CNS, presently confound interpretive acumen in regenerative studies.
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PMID:Myelin-, reactive glia-, and scar-derived CNS axon growth inhibitors: expression, receptor signaling, and correlation with axon regeneration. 1504 47