Stim1^−/− chimeras are protected from cerebral ischemia. (A, left) Representative images of three corresponding coronal sections from control mice and Stim1^−/− chimeras stained with TTC 24 h after tMCAO. Infarcts in Stim1^−/− chimeras are restricted to the basal ganglia (white arrow), in contrast to controls (black arrows). (right) Brain infarct volumes in controls (n = 7) and Stim1^−/− chimeras (n = 7). Values are mean ± SD. ***, P < 0.0001. Bar, 5 mm. (B and C) Neurological Bederson score and grip test assessed at day 1 after tMACO of controls (n = 7) and Stim1^−/− chimeras (n = 7). Values are mean ± SD. ***, P < 0.0001. (D) The coronal T2-w MR brain image shows a large hyperintense ischemic lesion at day 1 after tMCAO in controls (white arrows; top left). Infarcts are smaller in Stim1^−/− chimeras (white arrow; bottom left), and T2 hyperintensity decreases by day 7 during infarct maturation (white arrow; bottom right). Importantly, hypointense areas indicating intracerebral hemorrhage were not seen in Stim1^−/− chimeras, demonstrating that Stim1 deficiency does not increase the risk of hemorrhagic transformation, even at advanced stages of infarct development. Bar, 5 mm. (E) Hematoxylin and eosin–stained sections of corresponding territories in the ischemic hemispheres of control and Stim1^−/− chimeras. Infarcts are restricted to the basal ganglia in Stim1^−/− chimeras but consistently include the cortex in controls. Bars: (left) 200 μm; (right) 50 μm.