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. Author manuscript; available in PMC: 2018 Jan 3.
Published in final edited form as: Brain Res. 2016 Mar 25;1642:163–169. doi: 10.1016/j.brainres.2016.03.011

Figure 5. Summary diagram of MEP-mediated enhancement of synaptic NMDAR localization and upregulation of Prx2.

Figure 5

MEP increases phospho-activation of Src and Pyk2 by day 2 of treatment. These kinases are known to mediate synaptic localization of NMDARs by phosphorylation of their C-terminal regulatory domains, which occludes internalization by clathrin/AP2-mediated endocytosis. Increased expression of NMDAR subunits in combination with PSD-95 (Mitchell et al., 2009) results in enhanced synaptically-localized receptor complex. Synaptic NMDAR activity increases neuronal antioxidant defenses in the form of upregulating Prx2 and resultant neuroprotection. This pathway can be circumvented by D3T, which lends support to the speculation that naturally occurring phytochemicals in combination with extrasynaptic NMDAR blockers may act synergistically to combat redox stress-related neurodegenerative processes.