Fig. 1.

Formation of cortical lesion and hematoma regression after TBI are not affected by the pre-existing mLV dysfunction. (A) Representative coronal (upper panels) and axial (lower panels) reconstructed T1-weighted MRI images showing the hemorrhage extension in WT CCI and TG CCI brains, as recorded at 1 and 14 days post-TBI induction (dpi). Hematoma is visible at 1 dpi, and mostly regress by 14 dpi, in both TG and WT mice. (B–C) In vivo analysis of lesion formation. Longitudinal analyses of cortical and subcortical lesion volume ipsilateral to the site of injury and edema formation (swelling) show no genotype related differences. (D) Regression of the hematoma volume in TG and WT mice, analyzed at 1, 7 and 14 days after TBI. For the definitions of the hematoma volume see the main text. (E) Unfolded cortical map showing the mean lesion extension in WT- (orange) and TG-CCI (blue) mice. In both genotypes, CCI induction resulted in a similar lesion affecting prevalently the visual and somatosensory cortices. (F–G) Post-mortem histological analyses at 2 month post-TBI show similar lesions in the two genotypes. (F) Evaluation of the cortical area affected by the brain injury (unfolded cortical map quantification). (G) Cortical volume loss as evaluated ex vivo. Data analyses: Kruskal Wallis test with Sidak correction. A linear mixed-effect model (lme) was applied to assess statistical differences in the analysis of hematoma volume regression. dpi: days post injury, ML: mid line. For cortical area annotation, refer to Franklin and Paxinos mouse brain atlas (Franklin and Paxinos, 2007). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)