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Fig. 3 | Molecular Pain

Fig. 3

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

Fig. 3

Proposed model for the involvement of spinal cord mTOR in chronic opioid tolerance and hyperalgesia. Under normal conditions (a), mTOR is inactivated. 4E-BP1/2 binds to eIF4E, preventing its associations with the translation initiation complex, thus silencing protein translation. After repeated morphine exposure (b), activation of μ opioid receptors leads to the phosphorylation of PI3K and Akt, initiating a phosphorylation cascade including mTOR/S6K1/2/4E-BP1/2. eIF4E release, phosphorylated eIF4B, and phosphorylated S6 trigger protein translation. 4E-BP1/2: eIF4E-binding protein1/2. Akt: protein kinase B. eIF4E/eIF4B, eukaryotic translation initiation factor 4E/4B. mTOR: mammalian target of rapamycin. p: phosphorylated. PI3K: phosphoinositide 3-kinase. S6K1/2, p70 ribosomal S6 Kinase 1/2. S6K1, S6 Kinase 1. μ: μ opioid receptor

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