Abstract
The activation of mammalian target of rapamycin (mTOR), a serine/threonine protein kinase, has been known as one of the contributing factors in nociceptive sensitization after peripheral injury. Notably, its activation followed by the phosphorylation of downstream effectors causes the hyperexcitability of primary sensory neurons located in dorsal root ganglion (DRG). We investigated whether the inhibition of mTOR activation by directly injecting rAAV-shmTOR at the sciatic nerve of spared nerve injury (SNI) neuropathic pain model may decrease neuronal hyperexcitability in the DRG, along with downregulation of downstream effectors.
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