Following stroke, the damaged tissue undergoes liquefactive necrosis, a stage of infarct resolution that lasts for months although the exact length of time is currently unknown. One method of repair involves reactive astrocytes and microglia forming a glial scar to compartmentalize the area of liquefactive necrosis from the rest of the brain. The formation of the glial scar is a critical component of the healing response to stroke, as well as other central nervous system (CNS) injuries. The goal of this study was to evaluate the toxicity of the extracellular fluid present in areas of liquefactive necrosis and determine how effectively it is segregated from the remainder of the brain. To accomplish this goal, we used a mouse model of stroke in conjunction with an extracellular fluid toxicity assay, fluorescent and electron microscopy, immunostaining, tracer injections into the infarct, and multiplex immunoassays. We confirmed that the extracellular fluid present in areas of liquefactive necrosis following stroke is toxic to primary cortical and hippocampal neurons for at least 7 weeks following stroke, and discovered that although glial scars are robust physical and endocytic barriers, they are nevertheless permeable. We found that molecules present in the area of liquefactive necrosis can leak across the glial scar and are removed by a combination of paravascular clearance and microglial endocytosis in the adjacent tissue. Despite these mechanisms, there is delayed atrophy, cytotoxic edema, and neuron loss in regions adjacent to the infarct for weeks following stroke. These findings suggest that one mechanism of neurodegeneration following stroke is the failure of glial scars to impermeably segregate areas of liquefactive necrosis from surviving brain tissue.
Pubmed ID: 29331263 RIS Download
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Mus musculus with name C57BL/6J from IMSR.
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View all literature mentionsStatistical analysis software that combines scientific graphing, comprehensive curve fitting (nonlinear regression), understandable statistics, and data organization. Designed for biological research applications in pharmacology, physiology, and other biological fields for data analysis, hypothesis testing, and modeling.
View all literature mentionsThis polyclonal targets NG2 Chondroitin Sulfate Proteoglycan
View all literature mentionsThis monoclonal targets LAMP1
View all literature mentionsThis polyclonal targets Glial Fibrillary Acidic Protein
View all literature mentionsThis polyclonal targets Glial Fibrillary Acidic Protein
View all literature mentionsThis monoclonal targets Mouse CD68
View all literature mentionsThis polyclonal targets Glial Fibrillary Acidic Protein
View all literature mentionsThis polyclonal targets CD31
View all literature mentionsThis monoclonal targets LAMP1
View all literature mentionsThis monoclonal targets CD45R / B220
View all literature mentionsThis monoclonal targets Claudin 5
View all literature mentionsThis polyclonal targets Choline Acetyltransferase
View all literature mentionsThis polyclonal targets MMP9 - Whole molecule
View all literature mentionsThis polyclonal targets NG2 Chondroitin Sulfate Proteoglycan
View all literature mentionsThis polyclonal targets Iba1
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