As the resident immune cells in the central nervous system (CNS), microglia play an important role in maintaining homeostasis during development and in adult. After injury, macrophages arise from both the resident microglia and infiltrating monocytes, will migrate to the lesion site. It remains elusive whether the induced CNS regeneration can be influenced by manipulating the activity of microglia. PI3K/mTOR pathway is an important regulatory pathway related to the cell activity. Here, we used CX3CR1^CreER/+ mice line to specifically manipulate microglia. We found after the TSC1 knockout, the microglia become hypertrophic and hyperactive. In addition, TSC1 knockout in microglia inhibited the axon regeneration after the optic nerve crush. However, inactivation of microglia by manipulatin...[ Read more ]

As the resident immune cells in the central nervous system (CNS), microglia play an important role in maintaining homeostasis during development and in adult. After injury, macrophages arise from both the resident microglia and infiltrating monocytes, will migrate to the lesion site. It remains elusive whether the induced CNS regeneration can be influenced by manipulating the activity of microglia. PI3K/mTOR pathway is an important regulatory pathway related to the cell activity. Here, we used CX3CR1^CreER/+ mice line to specifically manipulate microglia. We found after the TSC1 knockout, the microglia become hypertrophic and hyperactive. In addition, TSC1 knockout in microglia inhibited the axon regeneration after the optic nerve crush. However, inactivation of microglia by manipulating the P85a, P110a, RAPTOR or mTOR didn’t influence axon regeneration. Our results suggest that the super active of microglia impair the axon regeneration.