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Original Article
- An Experimental Infarct Targeting the Internal Capsule: Histopathological and Ultrastructural Changes
- Chang-Woo Han, Kyung-Hwa Lee, Myung Giun Noh, Jin-Myung Kim, Hyung-Seok Kim, Hyung-Sun Kim, Ra Gyung Kim, Jongwook Cho, Hyoung-Ihl Kim, Min-Cheol Lee
- J Pathol Transl Med. 2017;51(3):292-305. Published online May 10, 2017
- DOI: https://doi.org/10.4132/jptm.2017.02.17
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- 5 Web of Science
- 6 Crossref
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Abstract
PDF - Background
Stroke involving the cerebral white matter (WM) has increased in prevalence, but most experimental studies have focused on ischemic injury of the gray matter. This study was performed to investigate the WM in a unique rat model of photothrombotic infarct targeting the posterior limb of internal capsule (PLIC), focusing on the identification of the most vulnerable structure in WM by ischemic injury, subsequent glial reaction to the injury, and the fundamental histopathologic feature causing different neurologic outcomes.
Methods
Light microscopy with immunohistochemical stains and electron microscopic examinations of the lesion were performed between 3 hours and 21 days post-ischemic injury.
Results
Initial pathological change develops in myelinated axon, concomitantly with reactive change of astrocytes. The first pathology to present is nodular loosening to separate the myelin sheath with axonal wrinkling. Subsequent pathologies include rupture of the myelin sheath with extrusion of axonal organelles, progressive necrosis, oligodendrocyte degeneration and death, and reactive gliosis. Increase of glial fibrillary acidic protein (GFAP) immunoreactivity is an early event in the ischemic lesion. WM pathologies result in motor dysfunction. Motor function recovery after the infarct was correlated to the extent of PLIC injury proper rather than the infarct volume.
Conclusions
Pathologic changes indicate that the cerebral WM, independent of cortical neurons, is highly vulnerable to the effects of focal ischemia, among which myelin sheath is first damaged. Early increase of GFAP immunoreactivity indicates that astrocyte response initially begins with myelinated axonal injury, and supports the biologic role related to WM injury or plasticity. The reaction of astrocytes in the experimental model might be important for the study of pathogenesis and treatment of the WM stroke. -
Citations
Citations to this article as recorded by
- Animal models of focal ischemic stroke: brain size matters
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Frontiers in Stroke.2023;[Epub] CrossRef - Motor Cortex Plasticity During Functional Recovery Following Brain Damage
Noriyuki Higo
Journal of Robotics and Mechatronics.2022; 34(4): 700. CrossRef - Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat
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International Journal of Molecular Sciences.2020; 21(17): 6246. CrossRef - Quantitative assessment of demyelination in ischemic stroke in vivo using macromolecular proton fraction mapping
Marina Y Khodanovich, Alena A Kisel, Andrey E Akulov, Dmitriy N Atochin, Marina S Kudabaeva, Valentina Y Glazacheva, Michael V Svetlik, Yana A Medvednikova, Lilia R Mustafina, Vasily L Yarnykh
Journal of Cerebral Blood Flow & Metabolism.2018; 38(5): 919. CrossRef - Immunosignals of Oligodendrocyte Markers and Myelin-Associated Proteins Are Critically Affected after Experimental Stroke in Wild-Type and Alzheimer Modeling Mice of Different Ages
Dominik Michalski, Anna L. Keck, Jens Grosche, Henrik Martens, Wolfgang Härtig
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Xiaohui Wang, Rongwen Li, Alex Zacharek, Julie Landschoot-Ward, Fengjie Wang, Kuan-Han Hank Wu, Michael Chopp, Jieli Chen, Xu Cui
International Journal of Molecular Sciences.2018; 19(11): 3368. CrossRef
- Animal models of focal ischemic stroke: brain size matters
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