Cited by 335Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsNeurological Disorders and Treatments

Oligodendrocytes and Ischemic Brain Injury

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Dewar, Deborah, Underhill, Suzanne M., Goldberg, Mark P.·2003·Journal of Cerebral Blood Flow & Metabolism

Abstract

Oligodendrocytes, myelin-forming glial cells of the central nervous system, are vulnerable to damage in a variety of neurologic diseases. Much is known of primary myelin injury, which occurs in settings of genetic dysmyelination or demyelinating disease. There is growing awareness that oligodendrocytes are also targets of injury in acute ischemia. Recognition of oligodendrocyte damage in animal models of ischemia requires attention to their distinct histologic features or use of specific immunocytochemical markers. Like neurons, oligodendrocytes are highly sensitive to injury by oxidative stress, excitatory amino acids, trophic factor deprivation, and activation of apoptotic pathways. Understanding mechanisms of oligodendrocyte death may suggest new therapeutic strategies to preserve or restore white matter function and structure after ischemic insults.

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Crossref · 10.1097/01.wcb.0000053472.41007.f9

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  • Oligodendrocytes express AMPA and kainate type glutamate receptors.

    “Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”

    From Neurocircuitry of Mood Disorders (2010) · cites this paper as Dewar et al, 2003

  • Oligodendrocytes are sensitive to excitotoxic damage from excess glutamate.

    “Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”

    From Neurocircuitry of Mood Disorders (2010) · cites this paper as Dewar et al, 2003

  • Oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate.

    “oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al. 2003; Matute et al. 1997; McDonald et al. 1998).”

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Research works printed but not linked: 1

  1. [105]105. Szuchet S (1995) The morphology and ultrastructure of oligodendro- cytes and their functional implications. In: Neuroglia (Kettnemann H, Ransom BR, eds), New York, NY: Oxford University Press, 23-43

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Authors
Dewar, D., Underhill, S. M., & Goldberg, M. P.
Affiliations
  • University of Glasgow (GB)
  • Washington University in St. Louis (US)
Venue
Journal of Cerebral Blood Flow & Metabolism
Published
2003-03
Volume
23
Issue
3
Pages
263-274
ISSN
  • 0271-678X (ISSN-L)
  • 1559-7016
OpenAlex
W2077440654
Cited by
335
References
123
Citations by year
2026: 11 · 2025: 11 · 2024: 17 · 2023: 17 · 2022: 14 · 2021: 18 · 2020: 19 · 2019: 20 · 2018: 12 · 2017: 9 · 2016: 24 · 2015: 25 · 2014: 10 · 2013: 23 · 2012: 15
FWCI
6.35
Type
journal article
Language
en
Open access
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
Funders
  • National Institutes of Health (5r01ns032626-04)
  • Medical Research Council
  • National Institute of Neurological Disorders and Stroke (NS 32626, NS36265, R01NS036265)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
oligodendrocytes, ischemic brain injury, myelin damage, demyelinating disease, acute cerebral ischemia, oxidative stress, excitatory amino acids, trophic factor deprivation, apoptosis, white matter preservation, immunocytochemical markers
MeSH terms
Animals, Brain Ischemia, Humans, Necrosis, Neurotoxins, Oligodendroglia, Apoptosis, Oxidative Stress, Neuroprotective Agents

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