Excitatory Amino Acid Receptors, Oxido-reductive Processes and Brain Oedema Following Transient Ischaemia in Gerbils

  • B. B. Mršulja
  • D. Stanimirović
  • D. V. Mićić
  • M. Spatz
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)


A key mechanism of brain injury after cerebral ischaemia is supposed to be the iron-dependent formation of highly reactive oxygen free radicals initiated by the intracellular accumulation of calcium and promoted by the excess release of glutamate. Oxido-reductive processes (formation of superoxide radicals and lipid peroxidation) are mediated through NMDA-receptors, while non-NMDA receptors, associated with (or being a part of) Na,K-ATPase, are responsible for postischaemic brain swelling. The hypothesis was put forward for consideration that release of glutamate (and other related endogenous excitatory amino acids) due to depolarization in the early minutes of ischaemia and (non)-NMDA antagonists may have roles in the development and prevention of metabolic brain impairment and cytotoxic oedema, respectively, in the ischaemic state.


Brain Oedema NMDA Antagonist Transient Ischaemia Excitatory Amino Acid Receptor Excitatory Amino Acid Release 
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Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • B. B. Mršulja
    • 1
  • D. Stanimirović
    • 2
  • D. V. Mićić
    • 1
  • M. Spatz
    • 3
  1. 1.Faculty of MedicineInstitute of BiochemistryBelgradeYugoslavia
  2. 2.Institute for Medical ResearchMilitary Medical AcademyBelgradeYugoslavia
  3. 3.LNNS, NINCDS, National Institutes of HealthBethesdaUSA

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