Roles of Calcium-Activated Enzymic Reactions in Ischemia-Induced Neuronal Injury

  • K. Kogure
  • H. Onodera
  • T. Tsuda
  • T. Araki
  • K. Nishioka
Conference paper

Abstract

Temporal ischemia of the brain injures only the selectively vulnerable brain cells. All of these neurons are constituents of either the limbic system or the basal ganglia, and recipients of the glutamatergic fibers. Recent studies in our laboratories unveiled that postischemic injury of these neurons is caused not by the energy failure but by dysfunction of the intracellular signal transducing system.

Keywords

Ischemia Dementia MgCl Diphenyl Inositol 

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References

  1. 1.
    Abe K, Kogure K, Yamada H, Imazawa M, Miyamoto K (1987) Mechanism of arachidonic acid liberation during ischemia in gerbil cerebral cortex. J Neurochem 48:503–509PubMedCrossRefGoogle Scholar
  2. 2.
    Kudo Y, Ogura A (1986) Glutamate-induced increase in intracellular Ca2+ concentration in isolated hippocampal neurones. Br J Pharmacol 89:191–198PubMedGoogle Scholar
  3. 3.
    Onodera H, Kogure K, Ono Y, Igarashi K, Kiyota Y, Nagaoka A (1988) Proto-oncogene c-fos is transiently induced in the rat cerebral cortex after forebrain ischemia. Neurosci LettGoogle Scholar
  4. 4.
    Suzuki R, Yamaguchi T, Choh-Luh Li, Klatzo I (1983) The effect of 5-minute ischemia in mongolian gerbils: II. Changes of spontaneous neuronal activity in cerebral cortex and CA1 sector of hippocampus. Acta Neuropathol (Berlin) 60:217–222CrossRefGoogle Scholar
  5. 5.
    Tsuda T, Kogure K, Ishii K, Orihara H (1988) Post-ischemic changes of calcium and endogenous antagonist in the rat hippocampus studied by proton induced X-ray emission analysis. Brain ResGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • K. Kogure
    • 1
  • H. Onodera
    • 1
  • T. Tsuda
    • 1
  • T. Araki
    • 1
  • K. Nishioka
    • 1
  1. 1.Department of NeurologyInstitute of Brain DiseasesSendai, 980Japan

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