• Neuroscience · Nov 2015

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

    • Y Izumi, M Sasaki, S Hashimoto, T Sawa, and F Amaya.
    • Department of Anesthesiology, Kyoto Prefectural University of Medicine, Japan.
    • Neuroscience. 2015 Nov 12; 308: 169-79.

    AbstractMammalian 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 2-4days after the incision. Rapamycin inhibited p-mTOR expression in the DRG and thermal hypersensitivity 3days but not 1day 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. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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