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. Author manuscript; available in PMC: 2018 Apr 1.
Published in final edited form as: Curr Opin Behav Sci. 2017 Apr;14:1–8. doi: 10.1016/j.cobeha.2016.09.012

Figure 2. Schematic representation of ketamine- and scopolamine- mediated disinhibition of mPFC pyramidal neurons via inhibition of local GABA interneurons.

Figure 2

Ketamine triggers a burst of glutamate that is thought to occur via inhibition of GABA interneurons; the tonic firing of these GABA interneurons is driven by NMDA receptors, and the active, open-channel state allows ketamine to enter and block channel activity. The resulting glutamate burst stimulates AMPA receptors, which causes depolarization and activation of voltage-dependent Ca2+ channels (VDCC), leading to release of BDNF and stimulation of TrkB and Akt, which then activates mTORC1 signaling, leading to the increased synthesis of proteins that are required for synapse maturation and formation (i.e., GluA1 and PSD95). Scopolamine also causes a glutamate burst via blockade of acetylcholine muscarinic M1 (ACh-M1) receptors on GABA interneurons.