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Results for “Cell Adhesion Molecules, Neuronal”

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PubMed2002

Evidence for a cell-specific action of Reelin in the spinal cord.

Reelin, the extracellular matrix protein missing in reeler mice, plays an important role in neuronal migration in the central nervous system. We examined the migratory pathways of phenotypically identified spinal cord neurons to determine whether their positions were altered in reeler mutants. Interneurons and projection neurons containing choline acetyltransferase and/or NADPH diaphorase were studied in E12.5-E17.5 reeler and wild-type embryos, and their final locations were assessed postnatally. While three groups of dorsal horn interneurons migrated and differentiated normally in reeler mice, the migrations of both sympathetic (SPNs) and parasympathetic preganglionic neurons (PPNs) were aberrant in the mutants. Initially reeler and wild-type SPNs were detected laterally near somatic motor neurons, but by E13.5, many reeler SPNs had mismigrated medially. Postnatally, 79% of wild-type SPNs were found laterally, whereas in reeler, 92% of these neurons were positioned medially. At E13.5, both reeler and wild-type PPNs were found laterally, but by E14.5, reeler PPNs were scattered across the intermediate spinal cord while wild-type neurons correctly maintained their lateral location. By postnatal day 16, 97% of PPNs were positioned laterally in wild-type mice; in contrast, only 62% of PPNs were found laterally in mutant mice. In E12.5-E14.5 wild-type mice, Reelin-secreting cells were localized along the dorsal and medial borders of both groups of preganglionic neurons, but did not form a solid barrier. In contrast, Dab1, the intracellular adaptor protein thought to function in Reelin signaling, was expressed in cells having positions consistent with their identification as SPNs and PPNs. In combination, these findings suggest that, in the absence of Reelin, both groups of autonomic motor neurons migrate medially past their normal locations, while somatic motor neurons and cholinergic interneurons in thoracic and sacral segments are positioned normally. These results suggest that Reelin acts in a cell-specific manner on the migration of cholinergic spinal cord neurons.

Animals↗

PubMed1990

Origin and distribution of enteric neurones in Xenopus.

In Xenopus, we investigated the origin of enteric neurones and their distribution in relation to the extracellular matrix (ECM) components, fibronectin (FN) and tenascin (TN). Enteric neurone precursor cells originate from the anterior trunk neural crest (NC). They migrate along the ventromedial NC pathway (between somites and neural tube/notochord) into the primitive gut (via the dorsal mesentery/lateral plate mesoderm) where they differentiate into enteric neurones. NC cells were identified during their migration and in the gut using the X. laevis - X. borealis nuclear marker system. The neuronal character of NC cells in the gut could be demonstrated immunohistochemically with a monoclonal antibody against the HNK-1 epitope. This antibody is superior to N-CAM and neurofilament antibodies which proved insufficient in Xenopus. In early tadpoles (stage 45), enteric neurones occurred frequently in the mesenchymal lining of the oesophagus, either singly or in groups of two to three cells. In more distal portions of the digestive tract, enteric neurones were rarely found. In metamorphosing tadpoles (stage 62/63), enteric neurones were scattered singly beneath the mucosa, or formed small aggregates between the inner and outer muscle layer throughout the length of the digestive tract. The neurones occurred in positions corresponding to the myenteric and submucosal plexus of higher vertebrates. The distribution of enteric neurones was studied in relation to fibronectin (FN) and tenascin (TN), glycoproteins of the ECM, which support (FN) and inhibit (TN) amphibian NC cell migration. Using immunohistochemistry, FN was found during NC cell migration in ECM spaces along the ventromedial pathway, and in the gut between the mucosa and the muscle layers, where it would be able to support adhesion and migration of NC cells. TN, in contrast, appeared much later than FN, both in the dorsal trunk and also ventrally, in the gut. In older tadpoles, TN was present in the mesenchyme and muscle layers of the digestive tract, where it might have an inhibiting influence on the migration of enteric neurones within the gut wall.

Animals↗

PubMed1992

L1 substrate enhances outgrowth of tyrosine hydroxylase-immunoreactive neurites in mesencephalic cell culture.

We have evaluated neurite outgrowth from mesencephalic tyrosine hydroxylase-positive neurons grown in vitro on different substrates. Cultures of ventral mesencephalon from rat embryos (E13) were plated on plastic dishes coated with the following substrates: L1, L2/HNK-1 "residual" (mainly J1/160 but also tenascin), MAG antigens from mouse brains, laminin, fibronectin, poly-L-lysine, RGD peptide, and plastic alone. After 3, 4, and 6 days in vitro, the cultures were stained using an antibody against tyrosine hydroxylase (TH), and the length of TH-positive neurites was measured by computer-assisted image analysis in a double-blind fashion. L1 antigen had a significant positive effect on neurite outgrowth compared to the other substrates studied. Laminin and fibronectin were also favorable substrates. In cultures treated with cytosine arabinoside to prevent mitoses and glial proliferation, the positive effect of L1 was abolished, but laminin still had a stimulatory effect. These data indicate that L1 may be indirectly involved in differentiation or axonal elongation of substantia nigra dopaminergic neurons and suggest a complex effect involving both neurons and glia on dopaminergic neurite development.

Animals↗

PubMed1995

Straying phenomenon of migrating LHRH neurons and highly polysialylated NCAM in the chick embryo.

The present study on unilaterally incompletely placodectomized chick embryos revealed that arrival of migrating LHRH neurons into the forebrain area is dependent on the presence of a central projection of the olfactory nerve. When a fragment of the lateral and medial olfactory epithelium was spared the damage, a small number of LHRH-ir cells were found to migrate into the forebrain along a thin NCAM-H-expressing fiber bundle of the olfactory nerve. In embryos with large lesions which destroyed the lateral olfactory epithelium, the poorly developed NCAM-H-positive olfactory nerve fibers were arrested where they meet the NCAM-positive medial nasal branch of the ophthalmic nerve and frequently fused with this branch fiber bundle. In these embryos, no LHRH-ir cells were detected in the forebrain area. They were deviated from their regular migratory course to the NCAM-H-positive medial nasal branch fiber bundle. This straying phenomenon indicates that some structural support is apparently needed for the migration of LHRH-ir cells, but their migratory route is not completely programmed in their precursor cells in the olfactory placode. In cultures of placodal tissues, the coexistence of migrating LHRH-ir cells with NCAM-H-expressing neural elements was always confirmed. It is suggested therefore that not only the structural support for the migration but also the interaction between LHRH-ir cells and NCAM-H-expressing neural elements is a prerequisite for successful LHRH neuronal migration.

Animals↗

PubMed2006

A novel mode of tangential migration of cortical projection neurons.

Projection neurons of the developing cerebral cortex are generated in the cerebral ventricular zone and subsequently move to the developing cortical plate via radial migration. Conversely, most inhibitory interneurons originate in the ganglionic eminences and enter the developing cortical plate by tangential migration. Using immunohistochemical analysis together with tracer labeling experiments in organotypic brain slices, we show that a portion of cortical projection neurons migrates tangentially over long distances. Lineage analysis revealed that these neurons are derived from Emx1+ cortical progenitors and express the transcription factor Satb2 but do not express GABA or Olig1. In vitro and in vivo analysis of reeler mutant brains demonstrated that although reeler mutation does not influence tangential migration of interneurons, it affects the tangential migration of cortical projection neurons.

Animals↗

PubMed2003

Neuroglian, Gliotactin, and the Na+/K+ ATPase are essential for septate junction function in Drosophila.

One essential function of epithelia is to form a barrier between the apical and basolateral surfaces of the epithelium. In vertebrate epithelia, the tight junction is the primary barrier to paracellular flow across epithelia, whereas in invertebrate epithelia, the septate junction (SJ) provides this function. In this study, we identify new proteins that are required for a functional paracellular barrier in Drosophila. In addition to the previously known components Coracle (COR) and Neurexin (NRX), we show that four other proteins, Gliotactin, Neuroglian (NRG), and both the alpha and beta subunits of the Na+/K+ ATPase, are required for formation of the paracellular barrier. In contrast to previous reports, we demonstrate that the Na pump is not localized basolaterally in epithelial cells, but instead is concentrated at the SJ. Data from immunoprecipitation and somatic mosaic studies suggest that COR, NRX, NRG, and the Na+/K+ ATPase form an interdependent complex. Furthermore, the observation that NRG, a Drosophila homologue of vertebrate neurofascin, is an SJ component is consistent with the notion that the invertebrate SJ is homologous to the vertebrate paranodal SJ. These findings have implications not only for invertebrate epithelia and barrier functions, but also for understanding of neuron-glial interactions in the mammalian nervous system.

Animals↗

PubMed2001

disabled-1 functions cell autonomously during radial migration and cortical layering of pyramidal neurons.

Genetic mosaics offer an excellent opportunity to analyze complex gene functions. Chimeras consisting of mutant and wild-type cells provide not only the avenue for lineage-specific gene rescue but can also distinguish cell-autonomous from non-cell-autonomous gene functions. Using an independent genetic marker for wild-type cells, we constructed Dab1(+/+) <--> Dab1(-/-) chimeras with the aim of discovering whether or not the function of Dab1 during neuronal migration and cortical layering is cell autonomous. Dab1(+/+) cells were capable of radial migration and columnar formation in a Dab1(-/-)environment. Most Dab1(+/+) cells segregated to the superficial part of the mutant cortex, forming a multilayered supercortex. Neuronal birth-dating studies indicate that supercortex neurons were correctly layered, although adjacent mutant cortex neurons were in reversed order. Immunocytochemistry using Emx1, a marker for pyramidal neurons, indicates that the vast majority of Dab1(+/+) neurons in the supercortex were Emx1 immunoreactive. Confirmation of the pyramidal phenotype was demonstrated by the absence of GABA immunoreactivity among Dab1(+/+) cells in the supercortex. Myelin staining using 2'3'-cyclic nucleotide 3'-phosphodiesterase showed the supercortex was supported by a secondary white matter from which thick fiber tracts appear connected to the underlying mutant white matter. The presence of Dab1(+/+) cells failed to rescue inversion of cortical layers and the abnormal infiltration of the marginal zone by Dab1(-/-) cells. Conversely, mutant cells did not impose a mutant phenotype on adjacent wild-type neurons. These results suggest that Dab1 functions cell autonomously with respect to radial migration and cortical layering of pyramidal neurons.

Adaptor Proteins, Signal Transducing↗

PubMed1990

An adherent subline of a unique small-cell lung cancer cell line downregulates antigens of the neural cell adhesion molecule.

Small-cell lung cancer (SCLC) lines are distinguished from non-small-cell lung cancer (NSCLC) lines by their growth in floating aggregates, in contrast to the adherent monolayers formed by NSCLC cells in culture. Of 50 well-characterized SCLC lines recently described by the National Cancer Institute (NCI)-Navy Medical Oncology Branch, only four variant cell lines (SCLC-v) grew as adherent monolayers. One line, NCI-H446, was unique in growing long-term with coexisting floating and surface adherent subpopulations. We have physically segregated these two populations over many passages in vitro to enrich for relatively pure cultures of floating and adherent cells. No differences in c-myc expression, keratin pattern, or cytogenetic appearance were found between the adherent and floating sublines. However, expression of the neuroendocrine marker neuron-specific enolase in the floating cells was three times that found in the adherent cells. The floating subline also had much greater surface expression of neuroendocrine tumor antigens detected by monoclonal antibodies UJ13A and HNK-1, which have been recently shown to detect the neural cell adhesion molecule (NCAM) on SCLC cells. Two other adherent SCLC-v lines were also found to be unreactive with UJ13A and HNK-1, generalizing the association between NCAM expression and the growth of most SCLC cultures as floating aggregates. In conclusion, we have an interesting model to study expression of NCAM as related to the adhesive properties of SCLC cells.

Antibodies, Monoclonal↗

PubMed2006

Stem cell properties of human periodontal ligament cells.

BACKGROUND AND OBJECTIVE: Stem cells have been used for regenerative therapies in various fields. The proportion of cells that possess stem cell properties in human periodontal ligament (PDL) cells is not yet well understood. In this study, we quantitatively characterized human PDL cells to clarify their stem cell properties, including self-renewal, multipotency, and stem cell marker expression. MATERIAL AND METHODS: PDL cells were obtained from extracted premolar or wisdom teeth, following which a proliferation assay for self-renewal, a differentiation assay for multipotency, immunostaining for STRO-1, and fluorescence-activated cell sorter (FACS) analysis for stem cell markers (including CD105, CD166, and STRO-1) were performed. RESULTS: Approximately 30% of 400 PDL cells were found to possess replicative potential and formed single-cell colonies, and 30% of these colonies displayed positive staining for STRO-1, 20% differentiated into adipocytes and 30% differentiated into osteoblasts. FACS analysis revealed that PDL cells, including cell populations, expressed the stem cell markers CD105, CD166, and STRO-1. CONCLUSION: The findings of this study indicated that PDL cells possess crucial stem cell properties, such as self-renewal and multipotency, and express the mesenchymal stem cell markers CD105, CD166, and STRO-1 on their cell surface, although there were some variations. Thus, PDL cells can be used for periodontal regenerative procedures.

Adipogenesis↗

PubMed2003

Increase in reelin-positive cells in the marginal zone of Pax6 mutant mouse cortex.

The extracellular matrix molecule reelin is a crucial molecule in CNS development, in particular in the cerebellum and cerebral cortex. In the cerebral cortex, reelin is provided by a small number of neurons located in the marginal zone (MZ). These neurons belong to the earliest neurons generated, but little is known about the molecular mechanisms of their specification. Here we describe that reelin-positive cells are strongly increased in the developing cortex of the Pax6 mutant mice Small eye. Shortly after the onset of reelin expression, the number of reelin- and calretinin-positive cells is doubled in the cortex of Pax6 mutants and this increase is further enhanced during development. In contrast, calbindin-positive cells in the MZ do not co-express reelin and are not altered in the Pax6 mutant cortex. The split of the preplate cells was also defective in the Pax6 mutant cortex, suggesting that the amount of reelin is crucial for positioning of the cortical plate between the MZ and subplate. We further show that Pax6 mutant cortical cells isolated in vitro do not develop an increase in reelin-positive cells, while cells isolated from the entire telencephalon do. Consistent with non-cell-autonomous mechanisms contributing to the increase in reelin-positive cells in the Pax6-deficient cortex, tangential migration of diverse cell types from the ventral telencephalon into the cortex is enhanced in the Pax6 mutant mice. Taken together, these experiments further elucidate how patterning of the forebrain by the transcription factor Pax6 regulates the specification of distinct neuronal subtypes in the cortical MZ.

Animals↗

PubMed1996

A nonneuronal isoform of cell adhesion molecule L1: tissue-specific expression and functional analysis.

The cell adhesion molecule L1 is a multifunctional protein in the nervous system characterizing cell adhesion, migration, and neurite outgrowth. In addition to full-length L1, we found an alternatively spliced variant lacking both the KGHHV sequence in the extracellular part and the RSLE sequence in the cytoplasmic part of L1. This L1 variant was expressed exclusively in nonneuronal cells such as Schwann cells, astrocytes, and oligodendrocytes, in contrast to the expression of the full-length L1 in neurons and cells of neuronal origin. To investigate the functions of the L1 variant, we established cell lines transfected with a cytoplasmic short L1 (L1cs) cDNA that lacks only the 12-bp segment encoding for the RSLE sequence. The promoting activities of homophilic cell adhesion, neurite outgrowth, and neuronal cell migration of L1cs-transfected cells (L4-2) were similar to those of full-length L1-transfected cells (L3-1), but the cell migratory activity of L4-2 itself was clearly lower than that of L3-1. In conclusion, the short form of L1 is a nonneuronal type, in contrast to the neuronal type of the full-length L1. Deletion of the four amino acids RSLE in the cytoplasmic region of L1 markedly reduced cell migratory activity, suggesting an importance of the RSLE sequence for the signaling events of neuronal migration mediated by L1.

Amino Acid Sequence↗

PubMed1990

Recombinant peripheral myelin protein P0 confers both adhesion and neurite outgrowth-promoting properties.

To probe into the functional properties of the major peripheral myelin cell surface glycoprotein P0, its ability to confer adhesion and neurite outgrowth-promoting properties was studied in cell culture. To this aim, P0 was expressed as integral membrane glycoprotein at the surface of CV-1 cells with the help of a recombinant vaccinia virus expression system. Furthermore, the immunoglobulin-like extracellular domain of P0 (P0-ED) was expressed as soluble protein in a bacterial expression system and used as substrate coated to plastic dishes or as competitor in cell adhesion and neurite outgrowth-promoting assays. The adhesion of P0-expressing CV-1 cells to P0-ED substrate was specifically inhibitable by polyclonal P0 antibodies (54% +/- 6%). In addition, the specific interaction between P0 molecules could be reduced (49% +/- 8%) by adding soluble P0-ED to the culture medium, demonstrating that the homophilic interaction between recombinant P0 molecules can be mediated, at least on one partner of interacting molecules, by the unglycosylated Ig-like domain. Substrate-coated P0-ED also conferred adhesion and neurite outgrowth ability to dorsal root ganglion neurons with neurites of a mean length of about 150 microns. This neurite outgrowth was specifically inhibitable by soluble P0 (74% +/- 14%) and P0 antibodies (65% +/- 9%). These observations indicate that P0 is capable of displaying two different types of functional roles in the myelination process of peripheral nerves: The heterophilic interaction with neurons may be responsible for the recognition between axon and myelinating Schwann cell at the onset of myelination, whereas the homophilic interaction may indicate its role in the self-recognition of the apposing loops of Schwann cell surface membranes during the myelination process and in the mature compact myelin sheath.

Animals↗

PubMed2006

Involvement of CD166 in the activation of human gamma delta T cells by tumor cells sensitized with nonpeptide antigens.

We previously reported that human Vgamma2Vdelta2-gammadelta T cells were activated by many human tumor cell lines treated with pamidronate (PAM) in a gammadelta TCR-dependent manner. In the present study, we indicated that a synthetic pyrophosphomonoester Ag, 2-methy-3-butenyl-1-pyrophosphate, could directly "sensitize" the tumor cells to activate gammadelta T cells independently of the host metabolism, while the sensitizing effect of PAM was reported to be dependent on the pharmacological activity. Some exceptional tumor cells that failed to be sensitized by PAM were incapable of activating gammadelta T cells by the treatment with 2-methy-3-butenyl-1-pyrophosphate either, suggesting a requirement of host factor(s) for the effective gammadelta T cell activation in addition to the nonpeptide Ags. By screening mAbs against a large panel of tumor cell lines, we found that the expression of CD166 closely paralleled the capacity of activating gammadelta T cells upon PAM treatment. The transfection of a CD166-negative tumor cell line with CD166 cDNA caused a marked enhancement of the capacity to activate gammadelta T cells following PAM treatment. On the contrary, down-regulation of the CD166 expression in a CD166-bearing tumor cell line by short hairpin RNA resulted in a significant reduction of PAM-induced gammadelta T cell-stimulatory activity. gammadelta T cells expressed CD6, a receptor of CD166, and CD6 and CD166 were recruited together to the center of synapse between gammadelta T cells and PAM-treated tumor cells, colocalizing with gammadelta TCR/CD3. The results suggested that the engagement of CD6 with CD166 on tumor cells played an important role in the gammadelta T cell activation by the tumor cells loaded with nonpeptide Ags either endogenously or exogenously.

Antibodies, Monoclonal↗

PubMed2005

The spermatogenic Ig superfamily/synaptic cell adhesion molecule mast-cell adhesion molecule promotes interaction with nerves.

Nerve-mast cell interaction is involved in both homeostatic and pathologic regulations. The molecules that sustain this association have not been identified. Because synaptic cell adhesion molecule (SynCAM), alternatively named spermatogenic Ig superfamily (SgIGSF), is expressed on both nerves and mast cells and because it binds homophilically, this molecule may be a candidate. To examine this possibility, mast cells with or without SgIGSF/SynCAM were cocultured with superior cervical ganglion neurons that express SgIGSF/SynCAM, and the number of mast cells attached to neurites was counted. The attachment of mast cells with SgIGSF/SynCAM, i.e., bone marrow-derived mast cells (BMMC) from wild-type mice, was inhibited dose-dependently by blocking Ab to SgIGSF/SynCAM. Mast cells without SgIGSF/SynCAM, i.e., BMMC from microphthalmia transcription factor-deficient mice and BMMC-derived cell line IC-2 cells, were defective in attachment to neurite, and transfection with SgIGSF/SynCAM normalized this. When the nerves were specifically activated by scorpion venom, one-quarter of the attached IC-2 cells mobilized Ca(2+) after a few dozen seconds, and ectopic SgIGSF/SynCAM doubled this proportion. At points of contact between neurites and wild-type BMMC, SgIGSF/SynCAM was locally concentrated in both neurites and BMMC. SgIGSF/SynCAM on mast cells appeared to predominantly mediate attachment and promote communication with nerves.

Animals↗

PubMed2006

Extracellular matrix and synaptic functions.

Comprehensive analysis of neuromuscular junction formation and recent data on synaptogenesis and long-term potentiation in the central nervous system revealed a number of extracellular matrix (ECM) molecules regulating different aspects of synaptic differentiation and function. The emerging mechanisms comprise interactions of ECM components with their cell surface receptors coupled to tyrosine kinase activities (agrin, integrin ligands, and reelin) and interactions with ion channels and transmitter receptors (Narp, tenascin-R and tenascin-C). These interactions may shape synaptic transmission and plasticity of excitatory synapses either via regulation of Ca2+ entry and postsynaptic expression of transmitter receptors or via control of GABAergic inhibition. The ECM molecules, derived from both neurons and glial cells and secreted into the extracellular space in an activity-dependent manner, may also shape synaptic plasticity through setting diffusion constraints for neurotransmitters, trophic factors and ions.

Agrin↗

PubMed2006

Mouse disabled 1 regulates the nuclear position of neurons in a Drosophila eye model.

Nucleokinesis has recently been suggested as a critical regulator of neuronal migration. Here we show that Disabled 1 (Dab1), which is required for neuronal positioning in mammals, regulates the nuclear position of postmitotic neurons in a phosphorylation-site dependent manner. Dab1 expression in the Drosophila visual system partially rescues nuclear position defects caused by a mutation in the Dynactin subunit Glued. Furthermore, we observed that a loss-of-function allele of amyloid precursor protein (APP)-like, a kinesin cargo receptor, enhanced the severity of a Dab1 overexpression phenotype characterized by misplaced nuclei in the adult retina. In mammalian neurons, overexpression of APP reduced the ability of Reelin to induce Dab1 tyrosine phosphorylation, suggesting an antagonistic relationship between APP family members and Dab1 function. This is the first evidence that signaling which regulates Dab1 tyrosine phosphorylation determines nuclear positioning through Dab1-mediated influences on microtubule motor proteins in a subset of neurons.

Animals↗

PubMed1991

Developmental expression of the axonal glycoprotein TAG-1: differential regulation by central and peripheral neurons in vitro.

TAG-1 is a 135,000 Mr axonal glycoprotein of the immunoglobulin superfamily that promotes axon extension in vitro. One distinguishing feature of TAG-1 is its transient expression on subsets of axons in the developing nervous system. To examine the mechanisms that regulate TAG-1, we have monitored the expression of this protein by developing central and peripheral neurons in vitro. TAG-1 was detected on the surface of a subset of E11 to E13 spinal cord neurons in vitro and was also released by these neurons. Expressions of TAG-1 on the cell surface was transient but it was possible to detect a released form of TAG-1 at all times in vitro. Spinal cord neurons isolated from older embryos did not express surface TAG-1 when they regenerated axons in vitro. Changes in the environment of spinal cord neurons did not alter the time course of TAG-1 expression, suggesting that regulation of the protein is cell autonomous. In contrast to these results with spinal cord neurons, surface expression of TAG-1 by DRG neurons persisted in vitro and adult DRG neurons re-expressed TAG-1 when grown in vitro. The cell surface and released forms of TAG-1 therefore appear to be regulated differently by central and peripheral neurons.

Animals↗

PubMed1991

The contrasting roles of N-CAM and N-cadherin as neurite outgrowth-promoting molecules.

The neural cell adhesion molecule (N-CAM) is a prominent member of the immunoglobulin gene superfamily of recognition molecules. It operates in a calcium-independent manner to promote cell-cell adhesion. Alternative splicing of a single gene generates more than twenty N-CAM isoforms and these can be further modified by the differential addition of complex N- and O-linked carbohydrates. In contrast, N-cadherin is a major calcium-dependent adhesion molecule in the brain; it is not a member of the immunoglobulin gene superfamily and, as far as we know, exists as a single gene product with no evidence of differential post-translational modification. Both molecules are believed to operate through a homophilic binding mechanism and both are expressed at key developmental times in a number of tissues including the brain. Antibody perturbation experiments suggest that both of the above cell adhesion molecules (CAMs) can support neurite outgrowth over complex cellular substrata such as astrocytes and Schwann cells. In the present review we discuss the use of a molecular genetic approach to study the neurite outgrowth-promoting activity of these molecules. Using this approach we have found that both CAMs are potent inducers of neurite outgrowth from a variety of neurons. However, whereas a critical value of N-CAM expression is required for increased neurite outgrowth, with small increases above this value having substantial effects, N-cadherin promotes neurite outgrowth in a highly linear manner. In addition, whereas N-CAM promotes chick retinal ganglion cell (RGC) neurite outgrowth at E6 but not E11, N-cadherin does so throughout this developmental period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗