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Fig. 2 | Molecular Pain

Fig. 2

From: mTOR, a new potential target for chronic pain and opioid-induced tolerance and hyperalgesia

Fig. 2

Proposed mechanism of spinal cord NMDA receptor-mediated activation of mTOR signaling in cancer pain. Under normal conditions (a), magnesium blocks NMDAR activity, thus silencing the intracellular kinases including the mTOR signaling pathway. Under cancer conditions (b), cancer-caused noxious insult leads to removal of the magnesium from NMDA receptors, resulting in calcium influx through NMDA receptor activation. The influx of calcium may then activate PI3K and Akt kinases which go on to phosphorylate mTOR. Active mTOR phosphorylates S6K1/2 and 4E-BP1/2 leading to protein translation initiation. 4E-BP1/2: eIF4E-binding protein1/2. Akt: protein kinase B. mTOR: mammalian target of rapamycin. NMDAR: NMDA receptor; NR1: a subunit of NMDA receptors. p: phosphorylated. PI3K: phosphoinositide 3-kinase. S6K1/2, p70 ribosomal S6 Kinase 1/2

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