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. 2017 Dec 22;21(4):371–381. doi: 10.1093/ijnp/pyx116

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© The Author(s) 2017. Published by Oxford University Press on behalf of CINP.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals. permissions@oup.com

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Figure 6. — Hypothetical mechanisms underlying the sustained antidepressant effects of ketamine. Ketamine increases serotonin (5-HT) release in the medial prefrontal cortex (mPFC) through local mechanisms such as inhibition of 5-HT transporter or through activation of the dorsal raphe nucleus (DRN) neurons by mPFC projection. Increase in 5-HT release may stimulate postsynaptic 5-HT_1A receptor in the mPFC, leading to activation of phosphoinositide-3 kinase (PI3K)/Akt/mTORC1 signaling. Activation of PI3K/Akt/mTORC1 signaling has been reported to mediate the sustained antidepressant effects of ketamine (Li et al., 2010).