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Photothrombotic Ischemia: A Minimally Invasive and Reproducible Photochemical Cortical Lesion Model for Mouse Stroke Studies
Published on: June 9, 2013
Histopathology of motor cortex in an experimental focal ischemic stroke in mouse model
Juçara Loli de Oliveira1, Pedro di Tárique Barreto Crispin2, Elisa Cristiana Winkelmann Duarte1
1Departamento de Ciências Morfológicas, Universidade Federal Santa Catarina, Brazil.
Abstract:
Experimental ischemia results in cortical brain lesion followed by ischemic stroke. In this study, focal cerebral ischemia was induced in mice by occlusion of the middle cerebral artery. We studied cortical layers I, II/III, V and VI in the caudal forelimb area (CFA) and medial agranular cortex (AGm) from control and C57BL/6 mice induced with ischemic stroke. Based on our analysis of CFA and AGm motor cortex, significant differences were observed in the numbers of neurons, astrocytes and microglia in the superficial II/III and deep V cortical layers. Cellular changes were more prominent in layer V of the CFA with nuclear pyknosis, chromatin fragmentation, necrosis and degeneration, as well as, morphological evidence of apoptosis, mainly in neurons. As result, the CFA was more severely impaired than the AGm in this focal cerebral ischemic model, as evidenced by the proliferation of astrocytes, potentially resulting in neuroinflammation by microglia-like cells.
Insights
Experimental ischemia causes brain lesions and stroke. This study found significant cellular changes in specific mouse motor cortex layers after middle cerebral artery occlusion, with the caudal forelimb area being more severely affected.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Cellular Biology
Background:
- Ischemic stroke, a major cause of brain damage, results from experimental ischemia.
- Understanding cortical layer-specific responses to focal cerebral ischemia is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the cellular and morphological changes in different cortical layers of the mouse motor cortex following focal cerebral ischemia.
- To compare the vulnerability of the caudal forelimb area (CFA) and medial agranular cortex (AGm) to ischemic injury.
Main Methods:
- Focal cerebral ischemia was induced in C57BL/6 mice via middle cerebral artery occlusion.
- Quantitative analysis of neurons, astrocytes, and microglia was performed in cortical layers I, II/III, V, and VI of the CFA and AGm.
- Histological examination assessed cellular damage, including apoptosis and necrosis.
Main Results:
- Significant differences in neuron, astrocyte, and microglia counts were observed between superficial (II/III) and deep (V) cortical layers in both CFA and AGm.
- Cortical layer V of the CFA exhibited more pronounced cellular damage, including nuclear pyknosis, chromatin fragmentation, necrosis, degeneration, and apoptosis, primarily in neurons.
- The CFA demonstrated more severe impairment compared to the AGm, indicated by astrocyte proliferation and potential neuroinflammation driven by microglia-like cells.
Conclusions:
- Focal cerebral ischemia differentially impacts cortical layers and brain regions, with layer V of the CFA being particularly vulnerable.
- Astrogliosis and microglial activation in response to ischemic injury suggest a role in neuroinflammation and potentially neuroprotection or exacerbation of damage.
- These findings highlight the complex cellular responses within the motor cortex following ischemic stroke and provide insights into region-specific vulnerabilities.
