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  • 1
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The presence of meningeal cells is necessary for the normal development of the glia limitans. Astrocytes comprising the adult glia limitans have several unique features, including many more gap junctions than is typical for astrocytes in the underlying molecular layer. This study examines the possible influence of meningeal cells on the establishment and maintenance of specific characteristics of astrocytes in the glia limitans. Primary cultures of rat astrocytes and meningeal cells were used to examine whether meningeal cells could alter astrocytic gap junctional dye coupling. Astrocytes and meningeal cells were grown on separate glass slides and co-cultured by forming a sandwich with the slides. The sides of the slides containing the cells faced each other and were separated by a 1 mm thick gasket along the edge of the slides. Although the meningeal cells and astrocytes were bathed in the same medium, they were separated by a distance of 1 mm and were not in direct contact during the co-culture period. The cells were co-cultured for 24, 48 or 72 hours, and astrocytic gap junctional dye coupling was examined using the gap-FRAP technique. The mean total recovery of fluorescence for control astrocytes was 14%. Astrocytes co-cultured with meningeal cells for 24 hours did not show a significant difference in the fluorescence recovery when compared to the control values. After 48 hours of co-culture, there was a significant increase in the gap junctional dye coupling. After 72 hours, gap junctional dye coupling continued to increase (total fluorescence recovery=53%). These results indicate that meningeal cells can influencein vitro gap junctional coupling. It is speculated that the prevalence of gap junctions in the glia limitans is due to-the meningeal-glial interaction.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurocytology 11 (1982), S. 1009-1029 
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Distinct aggregates of small intramembranous particles and assemblies characterize the P-face of freeze-fractured astrocytic membranes. To test the lability of the assemblies, astrocytes were treatedin vitro with different chemical agents andin vivo by cold injury. The assemblies appeared either to contain or be associated with protein because exposure to medium containing cycloheximide, an inhibitor of protein synthesis, led to a sharp decrease in assemblies, down to 1% of the control levels within three hours. To ascertain whether the assemblies were tethered to the cytoskeleton, the cells were treatedin vitro with disruptors of microtubules (colchicine) or microfilaments (cytochalasins); the assemblies became consistently rearranged. Protein denaturants, urea and guanidine HC1, brought about a selective aggregation of assembly with assembly. The lectin, concanavalin A, did not alter the distribution of the assemblies within the plane of the membrane fracture. Surface replicas ofin vitro, non-fractured, astrocytes revealed surface particles which did not resemble assemblies.In vivo, the plasma membranes of astrocytes were altered within minutes of cold injury to the brain surface. In the centre of the lesions, damaged astrocytes had assemblies that were clumped luce those ofin vitro astrocytes exposed to denaturants. In the periphery of the lesions, however, the assemblies did not aggregate but increased in number. These results provide indirect evidence that assemblies may consist of protein, that the recognizable particle constituent of the assembly is confined to the interior of the membrane and is not present on the uncleaved cell surface, and that assemblies are connected with the cytoskeleton. Therefore, certain changes in the environment of the astrocyte caused by injuryin vivo or addition of chemical agentsin vitro alter the distribution of assemblies in the astrocytic plasma membrane either by a direct effect on the assemblies or indirectly by an alteration of the cytoplasmic proteins.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurocytology 12 (1983), S. 767-784 
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mutant mouse strain Jimpy is characterized by a deficiency of myelin formation throughout the C.N.S. The cause of this hypomyelination is unknown. Based on previous reports, astrocytes, axons and oligodendrocytes are all altered, but no single cell type can be unequivocally defined as the primary target. Jimpy and age-matched normal mice were investigated using thin sectioning, freeze-fracturing and immunocytochemistry. We examined optic nerves and cervical spinal cords of Jimpy to determine which cells were morphologically altered during the period which precedes the onset of myelination and which cellular alterations persisted during myelinogenesis. Abnormalities of astrocytes and axons were frequently observed in Jimpy not only during myelination but also in early postnatal development before mature oligodendrocytes were present. The early astrocytic changes included hyperplasia and alterations of both cytoplasm and plasma membrane. An unusually complex network of astrocytic processes divided the axons into very small groups. During myelination, astrocytic processes were found insinuated between the axons and myelin sheath and/or within the myelin lamellae. Immunocytochemical investigations also revealed a complex network of glial fibrillary acidic protein-positive processes in contact with the majority of the axons. At stages prior to myelination axonal alterations were detected. Most of the axons were not in close contact with one another and individual axons had an undulating and irregular course. In areas where axon separation by astrocytic processes occurred, axonal diameters were more variable than the homogeneously sized axons of the normal mice. Our immunocytochemical results at stages during myelination showed not only many myelin basic protein-positive processes around axons in Jimpy but also clearly immunostained myelin sheaths. This indicates that the myelinating glia present not only produce myelin basic protein but can also incorporate it into the myelin spiral. The presented results suggest that the mouse mutant Jimpy could be a model for disturbed cell interactions in the C.N.S. Therefore, the hypomyelination may not be attributed to a defect of a single cell but rather to a deficiency in both macroglial types and, perhaps, the axon as well.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 256 (1989), S. 303-307 
    ISSN: 1432-0878
    Keywords: Arachnoid cells ; Tight and gap junctions ; Cold injury ; Ultrastructure ; Freeze-fracture technique ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The junctional complexes of cells in the outer arachnoid layer overlying the cerebral cortex of 2-week-old rats were examined with freeze-fracture electron microscopy up to 60 min after transcranial cold injury to the dorsal surface of the brain. Within 30 min after injury, areas of gap and tight junctions with morphological features characteristic of junction formation and/or junction disruption were found scattered among normal junctional complexes in some arachnoid cells. Within 60 min after injury, tight junctions with features typical of less leaky zonulae occludentes were present in all arachnoid cells examined. These morphological features include increases in the number of tight junctional strands and the number of strand-to-strand anatomoses. Gap junctions were interspersed among the tight junctional strands, and many were completely encircled by the strands. The increase in the number and complexity of the tight junctional strands in response to brain injury may be the morphological basis for the maintenance of the cerebrospinal fluid-blood dural barrier.
    Type of Medium: Electronic Resource
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