Background: Stroke models are essential tools in experimental stroke. Although several models of stroke have
been developed in a variety of animals, with the development of transgenic mice there is the need to develop a
reliable and reproducible stroke model in mice, which mimics as close as possible human stroke.
Methods: BALB/Ca-RAG2-/-gc-/- mice were subjected to cauterization or thrombosis stroke model and sacrificed at
different time points (48hr, 1wk, 2wk and 4wk) after stroke. Mice received BrdU to estimate activation of cell
proliferation in the SVZ. Brains were processed for immunohistochemical and EM.
Results: In both stroke models, after inflammation the same glial scar formation process and damage evolution
takes place. After stroke, necrotic tissue is progressively removed, and healthy tissue is preserved from injury
through the glial scar formation. Cauterization stroke model produced unspecific damage, was less efficient and
the infarct was less homogeneous compared to thrombosis infarct. Finally, thrombosis stroke model produces
activation of SVZ proliferation.
Conclusions: Our results provide an exhaustive analysis of the histopathological changes (inflammation, necrosis,
tissue remodeling, scarring...) that occur after stroke in the ischemic boundary zone, which are of key importance
for the final stroke outcome. This analysis would allow evaluating how different therapies would affect wound and
regeneration. Moreover, this stroke model in RAG 2-/- gC -/- allows cell transplant from different species, even
human, to be analyzed