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  • 1995-1999  (2)
  • 1975-1979  (1)
Materialart
Erscheinungszeitraum
Jahr
  • 1
    Digitale Medien
    Digitale Medien
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Neuroscience 19 (1996), S. 79-107 
    ISSN: 0147-006X
    Quelle: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Thema: Biologie , Medizin
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Journal of neurocytology 5 (1976), S. 691-718 
    ISSN: 1573-7381
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Regenerating neuromuscular junctions in the cutaneous pectoris muscle of the frog were examined by light and electron microscopy up to three months after crushing the motor nerve. The aim was to determine the precision of reinnervation of the original synaptic sites. More than 95% of the original postsynaptic membrane is recovered by nerve terminals and little, if any, synaptic contact is made on other portions of the muscle fibre surface. Even after prolonged denervation when the Schwann cells have retracted from 70–80% of the postsynaptic membrane, regenerating terminals return to and cover a large fraction of it. Although synapses are confined to the original synaptic sites, the pattern of innervation of muscle fibres is altered in several ways: (a) regenerating axon terminals can fail to branch leaving small stretches of postsynaptic membrane uncovered; (b) two terminal branches can lie side by side over a stretch of postsynaptic membrane normally occupied by one terminal; and (c) after growing along a stretch of postsynaptic membrane on one muscle fibre, terminals can leave it to end either in extracellular space or on the postsynaptic membrane of another fibre. Altogether the results demonstrate a strong and specific affinity between the original synaptic sites and regenerating nerve terminals.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Journal of inherited metabolic disease 20 (1997), S. 152-158 
    ISSN: 1573-2665
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Kennedy disease is a disorder with progressive motor neuron degeneration that is caused by trinucleotide repeat expansion in the androgen receptor gene. The disease mechanism likely involves toxicity of an expanded polyglutamine tract in the androgen receptor protein. This mechanism is probably shared by other neurodegenerative disorders with polyglutamine expansion, including Huntington disease. Attempts at reproducing the Kennedy disease phenotype by introducing the expanded androgen receptor into cultured neuronal cells and transgenic animals have thus far been unsuccessful, but recently developed model systems with other expanded polyglutamine constructs should allow the pathogenesis of these diseases to be elucidated.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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