Does Glutamatergic Excitatory Synaptic Transmission Play a Role in Ischemia?

  • D. Miller
  • S. J. Peerless
Conference paper


Glutamate and aspartate have become increasingly accepted by neurophysiologists as endogenous neurotransmitters. These acidic amino acids mediate excitatory synaptic transmission throughout the central nervous system. Three dendritic, postsynaptic receptor subtypes are known; a fourth possibly exists at a presynaptic site. The major excitatory amino acid receptors are named on the basis of specific agonist binding: N-methyl-D-aspartate (NMDA or NMA), Kainate, and Quisqualate. The non-NMDA receptors mediate fast, all-or-none excitatory transmission within glutamatergic pathways, whereas the NMDA receptors mediate such complex neurophysiological functions as long-term potentiation, memory, and learning.


NMDA Receptor Excitatory Amino Acid Transient Cerebral Ischemia Excitatory Amino Acid Receptor NMDA Recep 
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  1. 1.
    Benveniste H, Drejer J, Schousboe A, Diemer NH (1984) Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. J Neurochem 43:1369–1374PubMedCrossRefGoogle Scholar
  2. 2.
    Bosley TM, Woodhams PL, Gordon RD, Balazs R (1983) Effects of anoxia on the stimulated release of amino acid neurotransmitters in the cerebellum in vitro. J Neurochem 40:189–200PubMedCrossRefGoogle Scholar
  3. 3.
    Dingledine (1986) NMDA Receptors: What do they do? Trends Neurosci 9:47–49CrossRefGoogle Scholar
  4. 4.
    Excitatory Amino Acid Transmission, A Satellite Symposium to the XXX IUPS Congress, Abstract Volume, 20-23 July 1986Google Scholar
  5. 5.
    Fagg (1985) L-Glutamate, excitatory amino acid receptors and brain function. Trends Neurosci: 207-210Google Scholar
  6. 6.
    Fagg GE, Foster AC, Ganong AH (1986) Excitatory amino acid synaptic mechanisms and neurological function. Trends Pharmacol Sci 7:357–363CrossRefGoogle Scholar
  7. 7.
    French ED, Aldinio C, Schwarcz R (1982) Intrahippocampal kainic acid, seizures, and local neuronal degeneration: Relationships assessed in unanesthetized rats. Neuroscience 7:2525–2536PubMedCrossRefGoogle Scholar
  8. 8.
    Ikeda M, Yoshida S, Busto R, Santiso M, Ginsberg MD (1986) Polyphosphoinositides as a probable source of brain free fatty acids accumulated at the onset of ischemia. J Neurochem 47:123–132PubMedCrossRefGoogle Scholar
  9. 9.
    Mayer ML, Westbrook GL (1987) Cellular mechanisms underlying excitotoxicity. Trends Neurosci 10:59–61CrossRefGoogle Scholar
  10. 10.
    Meldrum B (1985) Excitatory amino acids and anoxic/ischemic brain damage. Trends Neurosci: 47-48Google Scholar
  11. 11.
    Meyer FB, Sundt TM Jr., Yanagihara T, Anderson RE (1987) Focal cerebral ischemia: Pathophysiologic mechanisms and rationale for future avenues of treatment. Mayo Clin Proc 62:35–55PubMedCrossRefGoogle Scholar
  12. 12.
    Nicoletti FM, Iadarola JT, Wroblewski T, Costa E (1986) Exicitatory amino acid recognition sites coupled with inositol phospholipid metabolism: Developmental changes and interaction with 1-adrenoceptors. Proc Natl Acad Sci USA 83:1931–1935PubMedCrossRefGoogle Scholar
  13. 13.
    Nicoletti F, Meek JL, Iadarola MJ, Chuang DM, Rothe BL, Costa E (1986) Coupling of inositol phospholipid metabolism with excitatory amino acid recognition sites in rat hippocampus. J Neurochem 46:40–46PubMedCrossRefGoogle Scholar
  14. 14.
    Nicoletti F, Wroblewski T, Novelli A, Alho H, Guidotti A, Costa E (1986) The activation of inositol phospholipid metabolism as a signaltransducing system for excitatory amino acids in primary cultures of cerebellar granule cells. J Neurosci 6:1905–1911PubMedGoogle Scholar
  15. 15.
    Rothman SM, Olney JW (1986) Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol 19:105–111PubMedCrossRefGoogle Scholar
  16. 16.
    Schwarcz R, Foster A, French E, Whetsell Köhler C (1984) Excitotoxic models for neurodegenerative disorders. Life Sci 35:19–32PubMedCrossRefGoogle Scholar
  17. 17.
    Schwarcz R, Meldrum, B (1985) Excitatory aminoacid antagonists provide a therapeutic approach to neurological disorders. Lancet 140-143Google Scholar
  18. 18.
    Siesjo BK (1984) Review article: Cerebral circulation and metabolism. J Neurosurg 60:883–908PubMedCrossRefGoogle Scholar
  19. 19.
    Simon RP, Swan JH, Griffiths T, Meldrum BS (1984) Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain. Science 226:850–852PubMedCrossRefGoogle Scholar
  20. 20.
    Watkins JC, Evans RH (1981) Excitatory amino acid transmitters. Ann Rev Pharmacol Toxicol 21:165–204CrossRefGoogle Scholar

Copyright information

© Springer Japan 1988

Authors and Affiliations

  • D. Miller
    • 1
  • S. J. Peerless
    • 1
  1. 1.Division of NeurosurgeryThe University of Western OntarioLondonCanada

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