Fig. 4
mTORC1 activation promotes ischemic brain injuries. a Assessment of mTORC1 activity in the brain after MCAO. Cerebral cortex samples were isolated from the contralateral or ipsilateral region at each indicated time point after MCAO, and the phosphorylation of p70S6k1 was compared by measuring the pp70S6k1(T389)/p70S6k1 ratio (n = 3). b mTORC1 activity in cerebral neurons after MCAO. Brain sections were prepared from mice 1 h after MCAO, and NeuN- or SNAT1 -positive cells in the cerebral cortex were double stained with an antibody against pp70S6k1(T389). Bars = 100 µm. c, d Inhibitory effect of neuron-specific Slc38a1 deficiency on mTORC1 activation by MCAO. Whole brain samples were isolated from control or mutant mice 1 h after MCAO, and pp70S6k1(T389) levels in the cerebral cortex were compared using immunohistochemistry c or western blotting (d, n = 3). Bars = 100 µm. e Suppression of the neuroprotective effect of Slc38a1 deficiency through Tsc1 heterozygosity. Whole brain samples were prepared from control, mutant, or mutant/Tsc1flox/wt mice after MCAO, and brain sections at the bregma were stained with an anti-MAP2 antibody to measure determine unstained areas (n = 3)
