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. 2013 Dec 27;4:161. doi: 10.3389/fphar.2013.00161

Figure 1.

Figure 1

Following blockade of NMDARs, phosphorylation of Akt activates mTOR complex 1 (mTORC1), which results in increased p70S6K phosphorylation and increased protein translation via inhibition of 4E-BP and release of eIF-4B. Glutamate binds AMPARs, which induces depolarization of the membrane, enabling Ca2+ influx through VDCCs. This results in BDNF release from synaptic vesicles. The subsequent binding of TrkB receptors induces ERK and Akt signaling. These pathways all converge to increase synaptic protein translation and receptor trafficking to the cell membrane. Additionally, activation of mTORC2 by S6, and inhibition of GSK-3, induces mTORC1 activation via increased Akt phosphorylation. Furthermore, mTORC2 activation induces protein kinase C (PKC) signaling transduction, which regulates actin and other cytoskeletal proteins.