The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.
Oligodendrocytes and Ischemic Brain Injury
Open accessAbstract
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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“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
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“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
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“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 Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression (2008) · cites this paper as Dewar et al. 2003
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Cites
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Cited by
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Drevets, W. C., Price, J. L., & Furey, M. L. (2008) · Brain Structure and Function · doi:10.1007/s00429-008-0189-x · Cited by 2,241
“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).”
BackgroundCampbell, B. C. V., Silva, D. A. D., Macleod, M. R., Coutts, S. B., Schwamm, L. H., Davis, S. M., & Donnan, G. A. (2019) · Nature Reviews Disease Primers · doi:10.1038/s41572-019-0118-8 · Cited by 1,965
Neurocircuitry of Mood Disorders
Price, J. L., & Drevets, W. C. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2009.104 · Cited by 1,606
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Neuroprotection for ischemic stroke: Past, present and future
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Metadata
- 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
- Publisher
- SAGE Publications
- 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
- bronze
- doi.org
- 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 › Neuroprotection in Cerebral Ischemia
- 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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