Excitotoxicity, free radicals, and cell membrane changes

Excitotoxicity, free radicals, and cell membrane changes Neuronal injury resulting from glutamate receptor–mediated excitotoxicity has been implicated in a wide spectrum of neurological disease states, including ischemia, central nervous system trauma, and some types of neurodegenerative diseases. Excitotoxicity may interact with other pathophysiological processes to enhance neuronal injury; for example, excess glutamate release due to free radicals generated during the immune response to infection might initiate secondary excitotoxicity, and intracellular pathways that contribute to neuronal destruction may be common to both excitotoxic and nonexcitotoxic injury processes. Defining the contribution of excitotoxicity to neuronal damage in acute zoster infection and post‐herpetic neuralgia may provide one means of reducing morbidity from this often debilitating disease. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Excitotoxicity, free radicals, and cell membrane changes

Annals of Neurology, Volume 35 (S1) – May 13, 1994

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Publisher
Wiley
Copyright
Copyright © 1994 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
D.O.I.
10.1002/ana.410350707
Publisher site
See Article on Publisher Site

Abstract

Neuronal injury resulting from glutamate receptor–mediated excitotoxicity has been implicated in a wide spectrum of neurological disease states, including ischemia, central nervous system trauma, and some types of neurodegenerative diseases. Excitotoxicity may interact with other pathophysiological processes to enhance neuronal injury; for example, excess glutamate release due to free radicals generated during the immune response to infection might initiate secondary excitotoxicity, and intracellular pathways that contribute to neuronal destruction may be common to both excitotoxic and nonexcitotoxic injury processes. Defining the contribution of excitotoxicity to neuronal damage in acute zoster infection and post‐herpetic neuralgia may provide one means of reducing morbidity from this often debilitating disease.

Journal

Annals of NeurologyWiley

Published: May 13, 1994

References

  • Glutamate and the pathophysiology of hypoxic‐ischemic brain damage
    Rothman, Rothman; Olney, Olney
  • Excitotoxic cell death
    Choi, Choi
  • Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis
    Benveniste, Benveniste; Drejer, Drejer; Schousboe, Schousboe; Diemer, Diemer
  • Regulation of glutamate and aspartate release from slices of the hippocampal CA1 area: effects of adenosine and baclofen
    Burke, Burke; Nadler, Nadler
  • Calmodulin is a subunit of nitric oxide synthase from macrophages
    Cho, Cho; Xie, Xie; Calaycay, Calaycay
  • Excitatory amino acid release from rat hippocampal slices as a consequence of free‐radical formation
    Pelligrini‐Giampietro, Pelligrini‐Giampietro; Cherici, Cherici; Alesani, Alesani

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