Figure 1.

The role of mTOR in neuronal survival following ischemia. (a) Under normal conditions, the adequate provision of nutrients and oxygen activates mTOR to stimulate anabolic processes such as protein synthesis while suppressing catabolic processes such as autophagy. (b) During stroke the reduction in provision of nutrients reduces mTOR activation, limiting protein synthesis and inducing autophagy. (c) Treatment of neurons with rapamycin can further reduce mTOR activation and increase the induction of autophagy. If autophagy induction is optimal this may lead to cell component recycling and cell survival (right-hand box). If autophagy is excessive, this may lead to apoptosis and cell death (left-hand box). mTORC1: mammalian target of rapamycin complex 1; S6K: S6kinase; S6rp: S6 ribosomal protein; 4EBP: eukaryotic translation initiation factor 4E binding protein; eIF4e: eukaryotic initiation factor 4e.