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Adhesion Molecule

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Urs Rutishauser – One of the best experts on this subject based on the ideXlab platform.

S.h Hrynkow – One of the best experts on this subject based on the ideXlab platform.

  • Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Craig Brumwell, Urs Rutishauser
    Abstract:

    Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.

  • Multiple roles of neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1 Adhesion Molecules during sensory innervation of the otic epithelium in vitro
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Masako M. Bilak, Urs Rutishauser
    Abstract:

    Abstract To explore the role of cell Adhesion Molecules in the innervation of the inner ear, antibody perturbation was used on histotypic co-cultures of the ganglionic and epithelial anlagen derived from the otocyst. When unperturbed, these tissues survived and differentiated in this culture system with outgrowth of fasciculated neuronal fibers which expressed neural cell Adhesion Molecule and L1. The fibers exhibited target choice and penetration, then branching and spreading within the otic epithelium as individual axons. Treatment of the co-cultures, or of the ganglionic anlagen alone, with anti-neural cell Adhesion Molecule or anti-L1 Fab fragments produced a defasciculation of fibers but did not affect neurite outgrowth. In the co-cultures this defasciculation was accompanied by a small increase in the number of fibers found in inappropriate tissues. However, the antibodies did not prevent fiber entry to the otic epithelium. In contrast, removal of polysialic acid from neural cell Adhesion Molecule with endoneuraminadase-N, while producing a similar fiber defasciculation, also increased the incidence of fibers entering the epithelium. Nevertheless, once within the target tissue, the individual fibers responded to either Fab or to desialylation by spreading out more rapidly, branching, and growing farther into the epithelium. The findings suggest that fasciculation is not essential for specific sensory fibers to seek out and penetrate the appropriate target, although it may improve their tracking efficiency. Polysialic acid on neural cell Adhesion Molecule appears to limit initial penetration of the target epithelium. Polysialic acid as well as neural cell Adhesion Molecule and L1 function are involved in fiber–target interactions that influence the arborization of sensory axons within the otic epithelium.

  • Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Craig Brumwell, Urs Rutishauser
    Abstract:

    Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.

J. Joseph Walshe – One of the best experts on this subject based on the ideXlab platform.

D. Kent Morest – One of the best experts on this subject based on the ideXlab platform.

  • Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Craig Brumwell, Urs Rutishauser
    Abstract:

    Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.

  • Multiple roles of neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1 Adhesion Molecules during sensory innervation of the otic epithelium in vitro
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Masako M. Bilak, Urs Rutishauser
    Abstract:

    Abstract To explore the role of cell Adhesion Molecules in the innervation of the inner ear, antibody perturbation was used on histotypic co-cultures of the ganglionic and epithelial anlagen derived from the otocyst. When unperturbed, these tissues survived and differentiated in this culture system with outgrowth of fasciculated neuronal fibers which expressed neural cell Adhesion Molecule and L1. The fibers exhibited target choice and penetration, then branching and spreading within the otic epithelium as individual axons. Treatment of the co-cultures, or of the ganglionic anlagen alone, with anti-neural cell Adhesion Molecule or anti-L1 Fab fragments produced a defasciculation of fibers but did not affect neurite outgrowth. In the co-cultures this defasciculation was accompanied by a small increase in the number of fibers found in inappropriate tissues. However, the antibodies did not prevent fiber entry to the otic epithelium. In contrast, removal of polysialic acid from neural cell Adhesion Molecule with endoneuraminadase-N, while producing a similar fiber defasciculation, also increased the incidence of fibers entering the epithelium. Nevertheless, once within the target tissue, the individual fibers responded to either Fab or to desialylation by spreading out more rapidly, branching, and growing farther into the epithelium. The findings suggest that fasciculation is not essential for specific sensory fibers to seek out and penetrate the appropriate target, although it may improve their tracking efficiency. Polysialic acid on neural cell Adhesion Molecule appears to limit initial penetration of the target epithelium. Polysialic acid as well as neural cell Adhesion Molecule and L1 function are involved in fiber–target interactions that influence the arborization of sensory axons within the otic epithelium.

  • Spatio-temporal diversity in the microenvironments for neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule expression by sensory neurons and their targets during cochleo-vestibular innervation
    Neuroscience, 1998
    Co-Authors: S.h Hrynkow, D. Kent Morest, Craig Brumwell, Urs Rutishauser
    Abstract:

    Abstract Sixteen phases in the microenvironments were defined for the structural development and innervation of the cochleo-vestibular ganglion and its targets. In each phase the cell Adhesion Molecules, neural cell Adhesion Molecule, neural cell Adhesion Molecule-polysialic acid, and L1-cell Adhesion Molecule, were expressed differentially by cochleo-vestibular ganglion cells, their precursors, and the target cells on which they synapse. Detected by immunocytochemistry in staged chicken embryos, in the otocyst, neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, was localized to the ganglion and hair cell precursors. Ganglionic precursors, migrating from the otocyst, only weakly expressed neural cell Adhesion Molecule. Epithelial hair cell precursors, remaining in the otocyst, expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule. Post-migratory ganglion cell processes expressed both Molecules in all stages. The cell Adhesion Molecules were most heavily expressed by axons penetrating the otic epithelium and accumulated in large amounts in the basal lamina. In the basilar papilla (cochlea), cell Adhesion Molecule expression followed the innervation gradient. Neural cell Adhesion Molecule and L1 were heavily concentrated on axonal endings peripherally and centrally. In the rhombencephalon, primitive epithelial cells expressed neural cell Adhesion Molecule, but not L1-cell Adhesion Molecule, except in the floorplate. The neuroblasts and their axons expressed L1-cell Adhesion Molecule, but not neural cell Adhesion Molecule, when they began to migrate and form the dorsal commissure. There was a stage-dependent, differential distribution of the cell Adhesion Molecules in the floorplate. Commissural axons expressed both cell Adhesion Molecules, but their polysialic acid disappeared within the floorplate at later stages. In conclusion, the cell Adhesion Molecules are expressed by the same cells at different times and places during their development. They are positioned to play different roles in migration, target penetration, and synapse formation by sensory neurons. A multiphasic model provides a morphological basis for experimental analyses of the Molecules critical for the changing roles of the microenvironment in neuronal specification.

Masato Kusunoki – One of the best experts on this subject based on the ideXlab platform.