Neurons of the peripheral nervous system are able to regenerate injured axons, a process requiring significant cellular resources to establish and maintain long-distance growth. Genetic activation of mTORC1, a potent regulator of cellular metabolism and protein translation, improves axon regeneration of peripheral neurons by an unresolved mechanism. To gain insight into this process, we activated mTORC1 signaling in mouse nociceptors via genetic deletion of its negative regulator Tsc2. Perinatal deletion of Tsc2 in nociceptors enhanced initial axon growth after sciatic nerve crush, however by three days post-injury axon elongation rate became similar to controls. mTORC1 inhibition prior to nerve injury was required to suppress the enhanced axon growth. Gene expression analysis in purified nociceptors revealed that Tsc2-deficient nociceptors had increased activity of regeneration-associated transcription factors (RATFs), including cJun and Atf3, in the absence of injury. Additionally, nociceptor deletion of Tsc2 activated satellite glial cells and macrophages in the dorsal root ganglia (DRG) in a similar manner to nerve injury. Surprisingly, these changes improved axon length but not percentage of initiating axons in dissociated cultures. The pro-regenerative environment in naïve DRG was recapitulated by AAV8-mediated deletion of Tsc2 in adult mice, suggesting that this phenotype does not result from a developmental effect. Consistently, AAV8-mediated Tsc2 deletion did not improve behavioral recovery after a sciatic nerve crush injury despite initially enhanced axon growth. Together, these data show that neuronal mTORC1 activation induces an incomplete pro-regenerative environment in the DRG that improves initial but not later axon growth after nerve injury. Long distance axon regeneration poses a significant hurdle to recovery following nervous system injury. Increased mTORC1 signaling improves axon regeneration, however the underlying mechanisms are incompletely understood. We activated neuronal mTORC1 signaling by genetically deleting Tsc2 in Nav1.8-positive neurons perinatally or by AAV8-mediated viral infection in adult mice and observed improved short- but not long-term axon regeneration after sciatic nerve injury. We suggest that Tsc2 deletion promotes initial but not later peripheral axon regeneration by upregulating expression of neuronal pro-regenerative genes and activating non-neuronal responses in the surrounding environment. Activating mTORC1 signaling in peripheral neurons may provide therapeutic benefit in circumstances with poor initial growth such as after spinal cord injury to the dorsal column or peripheral nerve repair.