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  • Glial plasmalemmal vesicles  (1)
  • Key words Glutamate  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The role of remaining presynaptic terminals in the hippocampal CA1 after selective neuronal death: ischemia-induced glutamate efflux (1995)
    Springer
    Acta neuropathologica 91 (1995), S. 41-46 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glutamate ; Ischemia ; Microdialysis ; Hippocampus ; Cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Following selective neuronal death, numerous presynaptic terminals maintain their structural integrity in the brain region. The role that these remaining presynaptic terminals play in the brain region showing selective neuronal death is not known. In the present study, we investigated the possibility that brief transient ischemia induces an excessive release of glutamate from the remaining presynaptic terminals, which then spreads by diffusion. The glutamate could act as an excitotoxin and be a pathogenic factor in the local injured brain region. Transient ischemia of 3.5 min duration was used in the gerbil as a pretreatment to obtain hippocampal CA1 in which most of postsynaptic neurons were eliminated but numerous presynaptic terminals remained normal. At 10–14 days after the pretreatment, brain microdialysis experiments were performed in vivo in the CA1 to measure the levels of extracellular glutamate induced by 5 min ischemia. Prior to 5 min ischemia the basal concentration of glutamate in the CA1 was the same as that observed in gerbils that had been subjected to sham pretreatment. During 5 min ischemia, no significant increase in glutamate was induced in the CA1 which showed selective neuronal death. However, a massive increase in glutamate was induced in the CA1 of the sham-pretreated gerbils. These results suggest that the remaining presynaptic terminals are unlikely to play a pathogenic role in the CA1 after selective neuronal death has occurred.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050390
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  • 2
    Electronic Resource
    Electronic Resource
    Uptake of transmitter amino acids by glial plasmalemmal vesicles from different regions of rat central nervous system (1994)
    Springer
    Neurochemical research 19 (1994), S. 1145-1150 
    Details
    ISSN: 1573-6903
    Keywords: Glial plasmalemmal vesicles ; glutamate ; γ-aminobutyric acid ; glycine ; Na+-dependent transport ; choline ; dopamine ; synaptosomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract From rat hippocampal homogenate, we recently isolated a novel subcellular fraction richly containing glial plasmalemmal vesicles (GPV), which takes up glutamate remarkably as a synaptosomal fraction [Y. Nakamura et al. (1993) Glia, 9, 48–56]. In the present study, we prepared GPV from different regions of rat CNS, namely olfactory bulb (Ob), cerebral cortex (Cx), caudatoputamen (Cp), hippocampus (Hp), cerebellum (Ce) and spinal cord (Sc), and analyzed their activities of Na+-dependent uptake of following neurotransmitters and a related compound; glutamate, γ-aminobutyrate (GABA), glycine, dopamine and choline. The uptake activities of these amino acids were not significantly different between GPV and synaptosomes in each region. Regionally, however, the activities were varied considerably. The activities of glutamate uptake revealed in the following rank order: Cx, Hp, Cp〉Ce, Ob〉Sc. GABA uptake activities were: Ce〉Ob, Cx, Hp〉Cp, while glycine uptake activities were: Sc, Ce〉Ob, Cp, Cx, Hp. On the other hand, the uptake activities of dopamine and choline were quite different between GPV and synaptosomes. Synaptosomal fraction from Cp took up dopamine in a high activity; however, GPV from the same tissue hardly showed the uptake activity. Choline was taken up by synaptosomes prepared from Hp but not by GPV.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00965148
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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