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  • Articles: DFG German National Licenses  (4)
  • Electronic Resource  (4)
  • 1985-1989  (4)
  • 1989  (4)
Source
  • Articles: DFG German National Licenses  (4)
Material
  • Electronic Resource  (4)
Years
  • 1985-1989  (4)
Year
  • 1
    ISSN: 1432-0533
    Keywords: Major histocompatibility complex ; Ia antigens ; Microglia ; Experimental allergic encephalomyelitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Monoclonal antibodies (MRC OX-6 and OX-17) recognized three types of cells expressing Ia antigen during the course of acute experimental allergic encephalomyelitis (EAE) in rats. In earlier stages of the disease, in animals with or without paralysis, Ia antigens were mostly localized to subarachnoidal and perivascular lymphocytic and histiocytic cell infiltrates, possibly serving as antigen-presenting cells. On the other hand, in convalescent rats, Ia antigens were expressed in a large number of cells with dendritic processes heavily populating the spinal gray matter. The appearance of these Ia-expressing cells in the convalescent stage coincided with the development of degenerating axon terminals in the spinal gray matter. These Ia-expressing cells possessed morphological features characteristic of microglia and were positive for ML-1 lectin but did not express glial fibrillary acidic protein. Immune electron microscopy disclosed the presence of Ia reaction products in the Golgi apparatus, endoplasmic reticulum and plasma membrane of these cells with dendritic processes, indicating active synthesis of Ia molecules in microglia. In addition, Ia antigens were localized to the cells with ultrastructural features of macrophages. Thus, Ia-expressing cells in EAE seems to play dual roles: the induction of immunological reactions during earlier stages and the participation in reparative processes during convalescence.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 77 (1989), S. 357-368 
    ISSN: 1432-0533
    Keywords: Hepatic encephalopathy ; Glutamine synthetase ; Methionine sulfoximine ; Oligodendrocyte ; Astrocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the roles imposed on astrocytes for glutamate metabolism, a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSO), was repeatedly administered to rats and histopathological changes were correlated with glycogen accumulation and the immunocytochemistry of GS and glial fibrillary acidic protein (GFAP). Prolonged MSO-loading (every 12 h up to three times, 100–150 mg/kg body weight) brought about the appearance of astrocytes with swollen, watery nuclei reminiscent of Alzheimer II glia chiefly in the neocortex, hippocampus and lateral thalamus after 24 h. Concomitantly, profound accumulation of glycogen ensued in the superficial three layers of the neocortex, hippocampus and pyriform cortex. GS immunoreactivity appeared enhanced in the cortex, hippocampus and lateral thalamus with parallel increase in GFAP immunoreactivity after prolonged treatment. Oligodendrocytes in the diencephalon and brain stem also normally contained GS immunoreactivity. Some animals developed necrotic lesions in the dorsolateral neocortex. The area of glycogen accumulation coincided with the known distribution ofN-methyld-aspartate (NMDA) glutamate receptors and, thus, GS may play important roles in NMDA receptor-mediated glutamate metabolism. The Alzheimer II type changes, however, did not correlate with NMDA-receptor distribution. These results indicate certain regionalizations in the roles of astrocytes and oligodendrocytes in glutamate and ammonia metabolisms.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 236 (1989), S. 373-374 
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 236 (1989), S. 186-187 
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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