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  • 2000-2004  (2)
  • 2002  (2)
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  • 2000-2004  (2)
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  • 1
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Glutamate release in ischaemia triggers neuronal death. The major glial glutamate transporter, GLT-1, might protect against glutamate-evoked death by removing extracellular glutamate, or contribute to death by reversing and releasing glutamate. Previous studies of the role of GLT-1 in ischaemia have often used the GLT-1 blocker dihydrokainate at concentrations that affect transporters other than GLT-1 and which affect kainate, N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors. In hippocampal slices from postnatal day 14 mice lacking GLT-1, the current response of area CA1 pyramidal cells to superfused AMPA and NMDA (which are not taken up) was unaffected, whereas the response to 100 µm glutamate was more than doubled relative to that in wild-type littermates, a finding consistent with a decrease in glutamate uptake. In response to a few minutes of simulated ischaemia, pyramidal cells in wild-type mice showed a large and sudden inward glutamate-evoked current [the anoxic depolarization (AD) current], which declined to a less inward plateau. In mice lacking GLT-1, the time to the occurrence of the AD current, its amplitude, the size of the subsequent plateau current and the block of the plateau current by glutamate receptor blockers were all indistinguishable from those in wild-type mice. We conclude that GLT-1 does not contribute significantly to glutamate release or glutamate removal from the extracellular space in early simulated ischaemia. These data are consistent with glutamate release being by reversal of neuronal transporters, and with uptake into glia being compromised by the ischaemia-evoked fall in the level of ATP needed to convert glutamate into glutamine.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 81 (2002), S. 1267-1269 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: A method for altering the local direction and angular dispersion of anisotropy in soft magnetic films using energetic ion irradiation is demonstrated. NiFe films 50 Å thick were irradiated with 200 keV Ar+ ions to doses between 1013 and 1016 ions/cm2, while a saturating magnetic field was applied to the samples. This annealing field defined the new anisotropy direction of the irradiated areas, and the irradiation process also led to changes in the angular dispersion of anisotropy orientation, as measured by angle-dependent remanence of magnetization. By appropriate masking of films, this technique has been used to pattern samples with small "anisotropy domains." © 2002 American Institute of Physics.
    Type of Medium: Electronic Resource
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