mTOR signaling controls VGLUT2 expression to maintain pain hypersensitivity after tissue injury

- mTOR is phosphorylated in the small-sized DRG neuron after the plantar incision.
- Inhibition of mTOR phosphorylation reduces thermal hyperalgesia after the plantar incision.
- Activation of mTOR signaling regulates VGLUT2 expression in the DRG.

Mammalian target of rapamycin (mTOR) is a serine-threonine protein kinase that controls protein synthesis in the nervous system. Here, we characterized the role of protein synthesis regulation due to mTOR signaling in rat dorsal root ganglion (DRG) following plantar incision. The number of phosphorylated mTOR (p-mTOR)-positive neurons was increased 2-4 days after the incision. Rapamycin inhibited p-mTOR expression in the DRG and thermal hypersensitivity 3 days but not 1 day after the incision. Vesicular glutamate transporter 2 (VGLUT2) expression was increased after the plantar incision, which was inhibited by rapamycin. These results demonstrated that tissue injury induces phosphorylation of mTOR and increased protein level of VGLUT2 in the DRG neurons. mTOR phosphorylation involves in maintenance of injury-induced thermal hypersensitivity.