Acute injury induces proliferation of reactive astrocytes and extensive intermingling of their elongated processes, forming glial scars surrounding damaged CNS tissues . Although glial scars limit damage in tissues, they may elicit seizures in patients after brain injury . Many factors generated by different cell sources influence scar formation . We employed a more severe injury model by stabbing mouse cortices with a sharp blade, and examined scars formed 7 and 15 days after injury (Figure 3d). Scar thickness was evaluated according to the immunoreactivity of GFAP plus that of AQP4, a membrane protein whose immunoreactivity labeled the full mormorphology of scar-forming astrocytes (Figure 3d and e). We found that astrocytic scars in the injured cortices of Mlc1-dnEGFR mice were formed thinner than those in littermate controls (Figure 3d and f). Thus, with the suppression on morphological expansion, scar formation ability of reactive astrocytes was impaired in Mlc1-dnEGFR mice.