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  • 1995-1999  (2)
  • Aspartate  (1)
  • Calcium  (1)
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  • 1995-1999  (2)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    In vitro ischemia-induced intracellular Ca2+ elevation in cerebellar slices: a comparative study with the values found in hippocampal slices (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 2-7 
    Details
    ISSN: 1432-0533
    Keywords: Calcium ; Ischemia ; Cerebellum ; Purkinje cell ; Microfluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in levels of intracellular calcium ion ([Ca2+]i) induced by in vitro ischemic conditions in gerbil cerebellar and hippocampal slices were investigated using a calcium imaging system and electron microscopy. When the cerebellar slice was perfused with a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (in vitro ischemic medium), a large [Ca2+]i elevation was region-specifically induced in the molecular laver of the cerebellar cortex (a dendritic field of Purkinje cells). When the hippocampal slice was perfused with in vitro ischemic medium, a large [Ca2+]i elevation was region-specifically induced in CA1 field of the hippocampal slices. Electron microscopic examinations showed that the large [Ca2+]i elevations occurred in Purkinje cells and CA1 pyramidal neurons. To isolate Ca2+ release from intracellular Ca2+ store sites, the slices were perfused with Ca2+-free in vitro ischemic medium. the increases in [Ca2+]i in both cerebellar and hippocampal slices were significantly lower than those observed in the slices perfused with the Ca2+-containing in vitro ischemic medium. However, the suppression of the [Ca2+]i-elevation in the molecular layer of the cerebellar slices was smaller than that in the CA1 field of the hippocampal slices. These results reinforce the hypothesis that calcium plays a pivotal role in the development of ischemia-induced neuronal death, and suggest that Ca2+ release from intracellular Ca2+ store sites may play an important role in the ischemia-induced [Ca2+]i elevation in Purkinje cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294252
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A possible mechanism for the hypoxia-hypoglycemia-induced release of excitatory amino acids from cultured hippocampal astrocytes (1995)
    Springer
    Neurochemical research 20 (1995), S. 737-743 
    Details
    ISSN: 1573-6903
    Keywords: Aspartate ; glutamate ; ischemic brain injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to elucidate the mechanism of release of excitatory amino acid (EAA) induced by hypoxiahypoglycemia (in vitro ischemia) from cultured hippocampal astrocytes, we compared the EAA release by in vitro ischemia with those by other treatments. The EAA release induced by in vitro ischemia treatment was rapid and reversible. The amount of released aspartate was comparable to that of glutamate, although the endogenous content of aspartate was one sixth that of glutamate. High-K (100 mM) treatment and the addition of 5 mM NaCN induced a rapid EAA release and the glutamate release was much greater than aspartate. Addition of 5 mM iodoacetate, a glycolysis inhibitor, induced a slow EAA release, and the amount of released aspartate was much higher than that of glutamate. On the other hand, the in vitro ischemia treatment and the addition of 5 mM NaCN induced only 20% reduction in ATP content for initial 5 min, whereas the addition of 5 mM iodiacetate induced a marked reduction. Our data suggest that ischemia-induced EAA release from astrocytes is a complex process in which local energy failure, inhibition of glycolysis, and depolarization of the cell membrane are involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01705543
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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