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  • 1
    Electronic Resource
    Electronic Resource
    Neurotransmitters in the spinal cord dorsal horn in a model of painful neuropathy and in nerve crush (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 478-485 
    Details
    ISSN: 1432-0533
    Keywords: Chronic constriction injury ; Crush ; Dorsal horn ; Hyperalgesia ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gammaaminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Metenk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-enk, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294809
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Neurotransmitters in the spinal cord dorsal horn in a model of painful neuropathy and in nerve crush (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 478-485 
    Details
    ISSN: 1432-0533
    Keywords: Key words Chronic constriction injury ; Crush ; Dorsal horn ; Hyperalgesia ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gamma-aminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Met-enk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-enk, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294809
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Increased lipocortin-1 (annexin-1) expression in the sciatic nerve of Lewis rats with experimental autoimmune neuritis (1999)
    Springer
    Acta neuropathologica 98 (1999), S. 583-589 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glucocorticosteroids ; Apoptosis ; Guillain-Barré syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lipocortin-1 exerts a potent immunosuppressive effect on pathogenic T cells. In multiple sclerosis and experimental autoimmune encephalomyelitis levels of lipocortins are raised, suggesting their involvement in the recovery from an immunological insult or in neural regeneration. To further understand the role of lipocortins in the peripheral nervous system we have characterized lipocortin-1 levels and cellular distribution of lipocortin-1 immunoreactivity in sciatic nerves of rats with experimental autoimmune neuritis (EAN), a model of human Guillain-Barré syndrome. EAN was induced actively by immunization with bovine peripheral myelin (active EAN) or by adoptive-transfer (AT-EAN) of P2-specific T cells. Cellular infiltrates in serial and semithin cryosections were characterized by immunohistochemistry. In parallel, lipocortin-1 levels in tissue extracts were quantified by a sandwich-ELISA. Only weak lipocortin-1 immunoreactivity was found in nerves of control animals injected with non-pathogenic T cells. The majority of macrophages and lymphocytes in EAN lesions exhibited lipocortin-1 immunoreactivity. Some very heavily stained cells showed a distribution and morphology similar to ED-2-positive macrophages which were abundant during early stages of EAN. Lipocortin-1 expression in T cells and macrophages was proven by immunocytochemical studies in semithin serial sections. In tissue extracts, lipocortin-1 levels increased from 0.24 ± 0.14 μg/mg protein in controls receiving non-pathogenic T cells to a maximum of 0.55 ± 0.1 μg/mg protein in AT-EAN at the peak of disease, and then slowly decreased during clinical recovery but still remained elevated. In dose-response studies in AT-EAN, highest values of lipocortin-1 (0.71 ± 0.23 μg/mg protein) were recorded after transfer of 2 × 107 T cells. Increased levels of lipocortin-1 were also measured in active EAN but occurred during the recovery phase (0.65 ± 0.27 μg/mg protein). By analogy with other immune-mediated disorders, increased lipocortin-1 expression in the inflamed sciatic nerve in EAN may exert immunoregulatory functions in-situ and contribute to the termination of the autoimmune response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051122
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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