GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Material
Publisher
Person/Organisation
Language
Years
FID
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Ensheathing the Node of Ranvier?
    Cambridge University Press (CUP) ; 2006
    In:  Neuron Glia Biology Vol. 2, No. 3 ( 2006-08), p. 149-150
    Details
    In: Neuron Glia Biology, Cambridge University Press (CUP), Vol. 2, No. 3 ( 2006-08), p. 149-150
    Type of Medium: Online Resource
    ISSN: 1740-925X , 1741-0533
    URL: Article
    DOI: 10.1017/S1740925X06000159
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2006
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Tenascin-R Promotes Neuronal Differentiation of Embryonic Stem Cells and Recruitment of Host-Derived Neural Precursor Cells After Excitotoxic Lesion of the Mouse Striatum
    Oxford University Press (OUP) ; 2008
    In:  Stem Cells Vol. 26, No. 8 ( 2008-08-01), p. 1973-1984
    Details
    In: Stem Cells, Oxford University Press (OUP), Vol. 26, No. 8 ( 2008-08-01), p. 1973-1984
    Abstract: Loss of GABAergic projection neurons under excitotoxic conditions in the striatum is associated with a disturbance of motor and cognitive functions as seen, for instance, in Huntington's disease. Since current treatments cannot replace degenerated neurons, research on alternative therapeutic approaches needs to be pursued. In this context, the transplantation of genetically modified stem cells into lesioned brain areas of patients is a possible alternative. In this study, green fluorescent protein-labeled murine embryonic stem cells (ESCs) were stably transfected to overexpress the extracellular matrix molecule tenascin-R (TNR), which is expressed by striatal GABAergic neurons. TNR-overexpressing ESCs were analyzed in comparison with their parental cells regarding neural differentiation and migration in vitro, and after transplantation into the striatum of quinolinic acid-treated mice, which serve as a model for Huntington's disease. In comparison with sham-transfected control cells, TNR-overexpressing ESCs showed enhanced differentiation into neurons in vitro, reduced migration in vitro and in vivo, and increased generation of GABAergic neurons and decreased numbers of astrocytes 1 month and 2 months after transplantation, but without significant effects on locomotor functions. Interestingly, TNR-overexpressing ESCs transplanted into the striatum attracted host-derived neuroblasts from the rostral migratory stream and promoted stem cell-mediated recruitment of host-derived newborn neurons within the grafted area. Thus, we show for the first time that overexpression of an extracellular matrix molecule by in vitro predifferentiated ESCs exerts beneficial effects on tissue regeneration in a mouse model of neurodegenerative disease. Disclosure of potential conflicts of interest is found at the end of this article.
    Type of Medium: Online Resource
    ISSN: 1066-5099 , 1549-4918
    URL: Article
    DOI: 10.1634/stemcells.2007-0929
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2008
    detail.hit.zdb_id: 2030643-X
    detail.hit.zdb_id: 1143556-2
    detail.hit.zdb_id: 605570-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    The Neural Cell Adhesion Molecule Promotes FGFR-Dependent Phosphorylation and Membrane Targeting of the Exocyst Complex to Induce Exocytosis in Growth Cones
    Society for Neuroscience ; 2011
    In:  The Journal of Neuroscience Vol. 31, No. 10 ( 2011-03-09), p. 3522-3535
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 31, No. 10 ( 2011-03-09), p. 3522-3535
    Abstract: The exocyst complex is an essential regulator of polarized exocytosis involved in morphogenesis of neurons. We show that this complex binds to the intracellular domain of the neural cell adhesion molecule (NCAM). NCAM promotes FGF receptor-mediated phosphorylation of two tyrosine residues in the sec8 subunit of the exocyst complex and is required for efficient recruitment of the exocyst complex to growth cones. NCAM at the surface of growth cones induces Ca 2+ -dependent vesicle exocytosis, which is blocked by an inhibitor of L-type voltage-dependent Ca 2+ channels and tetanus toxin. Preferential exocytosis in growth cones underlying neurite outgrowth is inhibited in NCAM-deficient neurons as well as in neurons transfected with phosphorylation-deficient sec8 and dominant-negative peptides derived from the intracellular domain of NCAM. Thus, we reveal a novel role for a cell adhesion molecule in that it regulates addition of the new membrane to the cell surface of growth cones in developing neurons.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3109-10.2011
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2011
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Neural Cell Adhesion Molecule-Mediated Fyn Activation Promotes GABAergic Synapse Maturation in Postnatal Mouse Cortex
    Society for Neuroscience ; 2013
    In:  The Journal of Neuroscience Vol. 33, No. 14 ( 2013-04-03), p. 5957-5968
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 33, No. 14 ( 2013-04-03), p. 5957-5968
    Abstract: GABAergic basket interneurons form perisomatic synapses, which are essential for regulating neural networks, and their alterations are linked to various cognitive dysfunction. Maturation of basket synapses in postnatal cortex is activity dependent. In particular, activity-dependent downregulation of polysialiac acid carried by the neural cell adhesion molecule (NCAM) regulates the timing of their maturation. Whether and how NCAM per se affects GABAergic synapse development is unknown. Using single-cell genetics to knock out NCAM in individual basket interneurons in mouse cortical slice cultures, at specific developmental time periods, we found that NCAM loss during perisomatic synapse formation impairs the process of basket cell axonal branching and bouton formation. However, loss of NCAM once the synapses are already formed did not show any effect. We further show that NCAM120 and NCAM140, but not the NCAM180 isoform, rescue the phenotype. Finally, we demonstrate that a dominant-negative form of Fyn kinase mimics, whereas a constitutively active form of Fyn kinase rescues, the effects of NCAM knockdown. Altogether, our data suggest that NCAM120/NCAM140-mediated Fyn activation promotes GABAergic synapse maturation in postnatal cortex.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1306-12.2013
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2013
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Prion Protein Regulates Glutamate-Dependent Lactate Transport of Astrocytes
    Society for Neuroscience ; 2007
    In:  The Journal of Neuroscience Vol. 27, No. 45 ( 2007-11-07), p. 12331-12340
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 45 ( 2007-11-07), p. 12331-12340
    Abstract: Prion-related protein (PrP) is a neural cell adhesion molecule involved in neurite outgrowth, neuronal survival, and synaptic function. In search of novel binding partners for PrP, we identified the α2/β2-Na + /K + -ATPase and showed that this astroglial ATPase interacts directly with the immunoglobulin superfamily adhesion molecule basigin. In cultured astrocytes, PrP is involved in regulating lactate transport via the astroglial monocarboxylate transporter 1 (MCT1) and in conjunction with α2/β2-ATPase and basigin. Lactate transport via MCT1 is glutamate dependent and regulated by glutamate receptor 2 (GluR2)-containing AMPA receptors with which PrP interacts. The functional interplay between PrP, GluR2, α2/β2-ATPase, basigin, and MCT1 in regulating lactate transport of astrocytes may be functional in the metabolic cross talk between astrocytes and neurons, most likely under stress.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1358-07.2007
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2007
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Close Homolog of L1 and Neuropilin 1 Mediate Guidance of Thalamocortical Axons at the Ventral Telencephalon
    Society for Neuroscience ; 2007
    In:  The Journal of Neuroscience Vol. 27, No. 50 ( 2007-12-12), p. 13667-13679
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 27, No. 50 ( 2007-12-12), p. 13667-13679
    Abstract: We report a cooperation between the neural adhesion molecule close homolog of L1 (CHL1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for establishment of area-specific thalamocortical projections. CHL1 deletion in mice selectively disrupted the projection of somatosensory thalamic axons from the ventrobasal (VB) nuclei, causing them to shift caudally and target the visual cortex. At the ventral telencephalon, an intermediate target with graded Sema3A expression, VB axons were caudally shifted in CHL1 − embryos and in Npn1 Sema−/− mutants, in which axons are nonresponsive to Sema3A. CHL1 colocalized with Npn1 on thalamic axons, and associated with Npn1 through a sequence in the CHL1 Ig1 domain that was required for Sema3A-induced growth cone collapse. These results identify a novel function for CHL1 in thalamic axon responsiveness to ventral telencephalic cues, and demonstrate a role for CHL1 and Npn1 in establishment of proper targeting of specific thalamocortical projections.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2888-07.2007
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2007
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Short‐Term Facilitation and Depression in the Cerebellum: Some Observations on Wild‐Type and Mutant Rodents Deficient in the Extracellular Matrix Molecule Tenascin C
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1048, No. 1 ( 2005-06), p. 185-197
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1048, No. 1 ( 2005-06), p. 185-197
    Abstract: A bstract : Short‐term plasticity was studied on synapses to Purkinje cells (PC): paired‐pulse facilitation in parallel fibers (PF) and paired‐pulse depression in climbing fibers (CF). Both phenomena relate to synaptic strength. These forms of short‐term plasticity were tested on cerebellar slices in rat by early postnatal synchronous stimulation of olivary neurons (i.e. CFs) with harmaline and by inhibition of a metabotropic glutamate receptor (mGluR) as well as in mice that were deficient in the extracellular matrix glycoprotein tenascin‐C. Harmaline stimulation delayed the developmental competition between CF inputs and maintained multiple innervation. Paired‐pulse depression of the CF‐PC synapse after harmaline treatment was more expressed. However, paired‐pulse facilitation in PF‐PC synapses remained unchanged. Electrophysiological responses of postsynaptic mGluR1 in CF‐PC synapses could be obtained only with AMPA receptors blocked and glutamate uptake impaired. The mGluR1‐specific antagonist CPCCOEt suppressed the CF‐mGluR EPSC in some PCs and potentiated it in other PCs. CF paired‐pulse depression was not changed with CPCCOEt, thus excluding a presynaptic effect. The postsynaptic effect was underlined by CPCCOEt‐induced rise in amplitude of EPSC and by a prolongation of its decay time. Tenascins are extracellular matrix glycoproteins that may restrict the regenerative capacity of the nervous tissue. Testing short‐term presynaptic plasticity in tenascin‐C‐deficient mice showed that CF paired‐pulse depression was less expressed while PF paired‐pulse facilitation was augmented except in a group of cells where there was even depression. The results underline differences in forms of short‐term plasticity with regard to susceptibility to diverse modulatory factors.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1342.017
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    The Cytoplasmic Domain of the Large Myelin-Associated Glycoprotein Isoform Is Needed for Proper CNS But Not Peripheral Nervous System Myelination
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 6 ( 1998-03-15), p. 1970-1978
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 6 ( 1998-03-15), p. 1970-1978
    Abstract: The myelin-associated glycoprotein (MAG) is a member of the immunoglobulin gene superfamily and is thought to play a critical role in the interaction of myelinating glial cells with the axon. Myelin from mutant mice incapable of expressing MAG displays various subtle abnormalities in the CNS and degenerates with age in the peripheral nervous system (PNS). Two distinct isoforms, large MAG (L-MAG) and small MAG (S-MAG), are produced through the alternative splicing of the primary MAG transcript. The cytoplasmic domain of L-MAG contains a unique phosphorylation site and has been shown to associate with the fyn tyrosine kinase. Moreover, L-MAG is expressed abundantly early in the myelination process, possibly indicating an important role in the initial stages of myelination. We have adapted the gene-targeting approach in embryonic stem cells to generate mutant mice that express a truncated form of the L-MAG isoform, eliminating the unique portion of its cytoplasmic domain, but that continue to express S-MAG. Similar to the total MAG knockouts, these animals do not express an overt clinical phenotype. CNS myelin of the L-MAG mutant mice displays most of the pathological abnormalities reported for the total MAG knockouts. In contrast to the null MAG mutants, however, PNS axons and myelin of older L-MAG mutant animals do not degenerate, indicating that S-MAG is sufficient to maintain PNS integrity. These observations demonstrate a differential role of the L-MAG isoform in CNS and PNS myelin.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.18-06-01970.1998
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Tenascin-R Inhibits the Growth of Optic Fibers In Vitro But Is Rapidly Eliminated during Nerve Regeneration in the Salamander Pleurodeles waltl
    Society for Neuroscience ; 1999
    In:  The Journal of Neuroscience Vol. 19, No. 2 ( 1999-01-15), p. 813-827
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 19, No. 2 ( 1999-01-15), p. 813-827
    Abstract: Tenascin-R is a multidomain molecule of the extracellular matrix in the CNS with neurite outgrowth inhibitory functions. Despite the fact that in amphibians spontaneous axonal regeneration of the optic nerve occurs, we show here that the molecule appears concomitantly with myelination during metamorphosis and is present in the adult optic nerve of the salamander Pleurodeles waltl by immunoblots and immunohistochemistry. In vitro , adult retinal ganglion cell axons were not able to grow from retinal explants on a tenascin-R substrate or to cross a sharp substrate border of tenascin-R in the presence of laminin, indicating that tenascin-R inhibits regrowth of retinal ganglion cell axons. After an optic nerve crush, immunoreactivity for tenascin-R was reduced to undetectable levels within 8 d. Immunoreactivity for the myelin-associated glycoprotein (MAG) was also diminished by that time. Myelin was removed by phagocytosing cells at 8–14 d after the lesion, as demonstrated by electron microscopy. Tenascin-R immunoreactivity was again detectable at 6 months after the lesion, correlated with remyelination as indicated by MAG immunohistochemistry. Regenerating axons began to repopulate the distal lesioned nerve at 9 d after a crush and grew in close contact with putative astrocytic processes in the periphery of the nerve, close to the pia, as demonstrated by anterograde tracing. Thus, the onset of axonal regrowth over the lesion site was correlated with the removal of inhibitory molecules in the optic nerve, which may be necessary for successful axonal regeneration in the CNS of amphibians.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.19-02-00813.1999
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1999
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Mice Deficient for Tenascin-R Display Alterations of the Extracellular Matrix and Decreased Axonal Conduction Velocities in the CNS
    Society for Neuroscience ; 1999
    In:  The Journal of Neuroscience Vol. 19, No. 11 ( 1999-06-01), p. 4245-4262
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 19, No. 11 ( 1999-06-01), p. 4245-4262
    Abstract: Tenascin-R (TN-R), an extracellular matrix glycoprotein of the CNS, localizes to nodes of Ranvier and perineuronal nets and interacts in vitro with other extracellular matrix components and recognition molecules of the immunoglobulin superfamily. To characterize the functional roles of TN-R in vivo , we have generated mice deficient for TN-R by homologous recombination using embryonic stem cells. TN-R-deficient mice are viable and fertile. The anatomy of all major brain areas and the formation and structure of myelin appear normal. However, immunostaining for the chondroitin sulfate proteoglycan phosphacan, a high-affinity ligand for TN-R, is weak and diffuse in the mutant when compared with wild-type mice. Compound action potential recordings from optic nerves of mutant mice show a significant decrease in conduction velocity as compared with controls. However, at nodes of Ranvier there is no apparent change in expression and distribution of Na + channels, which are thought to bind to TN-R via their β2 subunit. The distribution of carbohydrate epitopes of perineuronal nets recognized by the lectin Wisteria floribunda or antibodies to the HNK-1 carbohydrate on somata and dendrites of cortical and hippocampal interneurons is abnormal. These observations indicate an essential role for TN-R in the formation of perineuronal nets and in normal conduction velocity of optic nerve.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.19-11-04245.1999
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1999
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...