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  • Articles: DFG German National Licenses  (4)
  • Rat  (4)
  • Peripheral nervous system  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 78 (1989), S. 264-269 
    ISSN: 1432-0533
    Keywords: Skeletal muscle ; Regeneration ; Growth factors ; Growth hormone ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Against the background of the importance of growth hormone (GH) for normal muscle growth, a study was performed to investigate whether lack of GH after hypophysectomy affects the cell proliferation and the local production of insulin-like growth factor-I (IGF-I) in the early stages of muscle regeneration in adult rats. The level of IGF-I in the serum of hypophysectomised rats was reduced to about 30% of that of controls. The incorporation of [methyl-3H]thymidine into the regenerating muscle showed a peak 6 days after the operation and then gradually declined to the end of the period of study 30 days after initiation of regeneration by ischemic necrosis. The DNA content rose to a maximum level after 6–8 days, and remained high after 30 days. There was no major difference in the incorporation of [3H]thymidine in regenerating muscle of hypophysectomised and control rats, but the DNA concentration in the regenerating muscles of hypophysectomised rats was significantly reduced after 30 days. There was a corresponding reduction in the number of nuclei per muscle fibre, indicating that hypophysectomy has a small effect on the cell proliferation during the early stages of muscle regeneration. Immunohistochemical demonstration of IGF-I in the regenerating muscle revealed the transient presence of immunoreactive material in satellite cells and myotubes after 6 to 8 days of regeneration but no immunoreactivity after 30 days. No obvious difference was observed between hypophysectomised and control rats, indicating that the endogenous production of IGF-I in regenerating skeletal muscle can occur independently of GH.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 57 (1982), S. 1-6 
    ISSN: 1432-0533
    Keywords: Rat ; Malnutrition ; Protein deprivation ; Peripheral nervous system ; Ultrastructure ; Degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a previous study the occurrence of nerve fibre degeneration with a distribution as in dying-back neuropathies was described in young rats subjected to severe protein deprivation (Oldfors 1981). In this study the ultrastructural appearance of the degeneration of the nerve fibres at different levels of the longitudinal tail nerves in severely protein-deprived rats has been investigated. Various structural changes were noted, the most common being bands of Büngner indistinguishable from those seen in Wallerian degeneration. In nerve fibres which were less severely affected the most common finding was shrinkage of the axon with concomitant folding of the myelin sheath. Other structural changes included axonal accumulation of 10 nm filaments or mitochondria and other cell organelles, areas of demyelination, and projections of axolemma and Schwann cell membrane into the axon. Signs of axonal regeneration occurred but were infrequent. The degenerative changes seen at various levels of the nerves support the view that the neuropathy is of distal axonal type, but the structural appearance differs from several of the toxic dying-back neuropathies.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 54 (1981), S. 121-127 
    ISSN: 1432-0533
    Keywords: Rat ; Protein deprivation ; Nerve fibre degeneration ; Central nervous system ; Peripheral nervous system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Knowledge from previous reports that kwashiorkor in man may lead to nerve fibre degeneration prompted this study on rats. The rats were subjected to severe protein deprivation from 6 weeks of age. Protein deprivation was achieved by feeding the rats ad lib with a diet containing only 1.5% protein. Control rats received an iso-caloric diet with 14% protein. The vitamin content in both diets was well above normal requirements. In relation to body weight the protein-deprived rats did not consume less food than the control rats. Protein deprivation resulted in stunted body growth, markedly reduced values of serum albumin, and changes in the fur accompanied by areas of alopecia. Furthermore, the protein-deprived rats showed degeneration of nerve fibres in the medial parts of the posterior columns of the cervical but not the sacral part of the spinal cord and nerve fibre degeneration in the distal but not the proximal parts of the longitudinal tail nerves. Teased nerve fibre preparations of the tail nerves revealed changes consistent with the Wallerian type of degeneration. It is concluded that severe protein deprivation in young rats may lead to a “dying-back” type of neuropathy in the central and peripheral nervous systems.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Perineurium ; Protein deprivation ; Rat ; Peripheral nerve ; Diphtheria toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diphtheria toxin was locally administered around the sciatic nerves of normal and protein deprived rats aged 3, 6, 12, and 26 weeks in order to investigate the permeability of the barriers enveloping the nerves. At all ages the rats developed a reversible hind limb paralysis linked to a severe segmental demyelination, indicating passage of the toxin into the endoneurium. From 6 weeks of age the pattern of reaction differed between the protein deprived and control rats. The differences are discussed and interpreted as being partly dependent on less efficient protective barriers of the sciatic nerves of the protein deprived rats.
    Type of Medium: Electronic Resource
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