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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 75 (1987), S. 77-84 
    ISSN: 1432-0533
    Keywords: Wallerian degeneration ; Myelin phagocytosis ; Macrophages ; Millipore diffusion chambers ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Myelin phagocytosis in Wallerian degeneration was studied using a model of murine sciatic nerve degeneration in millipore diffusion chambers in the peritoneal cavity of host mice. Immunocytological investigations showed the dependence of myelin digestion on the invasion of Fc-positive, Mac-1-positive and partly Ia-positive monocytes. Lymphocytes did not play a prominent role. Compared to Wallerian degeneration in situ, phagocytosis was decreased in nerves enclosed by millipore membranes on both sides of the chamber. The membrane acted as a trap for invading monocytes/macrophages. Neither tissue integrity nor genetic strain influenced the degree of phagocytosis. A modification of the experimental technique is introduced which permits myelin phagocytosis in the peritoneal cavity in a degree comparable to that in Wallerian degeneration in situ.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 80 (1990), S. 415-418 
    ISSN: 1432-0533
    Keywords: Myelin phagocytosis ; Macrophages ; Complement receptor type 3 ; Organ culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Myelin phagocytosis in Wallerian degeneration of peripheral nerves depends on invasion of nerves by non-resident macrophages. The present study was done to clarify the role of the macrophage complement receptor type 3 (CR3) in myelin removal. Myelin phagocytic capacity of invading macrophages was abolished by treatment of cultured nerves and macrophages with anti-CR3 antibody or by serum complement depletion with cobra venom factor. This indicates that myelin phagocytosis is mediated by the macrophage CR3.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 66 (1985), S. 253-263 
    ISSN: 1432-0533
    Keywords: Angiogenesis ; Micrencephaly ; MAMAc
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The angiogenesis of the rat cerebrum was studied under pathologic conditions caused by the administration of the neurotoxin methylazoxymethanol acetate (MAMAc) in the time (E14) of neuroblast migration. The sinovenous junction of the main superficial cerebral veins and the morphological changes of the veins were examined by a quantitative analytic method. The hypoplastic areas of the brains showed extremely malformed venous systems with pathologic changes of the sinovenous junctions depending on the degree of disturbance of the neuroblast migration. These findings suggest the primary role of the neuronal maturation in the angioarchitectonic development and the direct dependency of the vascular differentiation on the neuroblast migration of the drained territory.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 68 (1985), S. 59-64 
    ISSN: 1432-0533
    Keywords: Angiogenesis ; Micrencephaly ; MAMAc
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The angioarchitecture of the superficial and basal arterial system of the hypoplastic rat brain caused by the administration of the neurotoxin, methylazoxymethanol acetate (MAMAc), at the time of neuroblast migration was studied. Increased variation of the arterial branching of the basal main stem of arteries and local vessel changes were observed. The findings suggest a close relationship between vascular and neuronal development, showing a generalized disturbance and local adaptation of vasculature to the altered neuronal architecture of the corresponding hypoplastic areas.
    Type of Medium: Electronic Resource
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