MK-801, but not anisomycin, inhibits the induction of tolerance to ischemia in the gerbil hippocampus
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Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke
2015, Experimental NeurologyCitation Excerpt :Other key mediators which have been involved in synaptic NMDA receptor-dependent neuroprotection include cyclic AMP responsive element binding protein, phosphatidylinositol 3 (PI3)-kinase, Akt and glycogen synthase kinase 3 beta (GSK3β). These mediators can be induced only by low doses of NMDA via the action potential-dependent route (Kato et al., 1992c; Raval et al., 2003). In addition, glutamate transporter-1 (GLT-1), a predominant subtype of glutamate transporter, has an important role in glutamate regulation.
Preconditioning effects of tumor necrosis factor-α and glutamate on calcium dynamics in rat organotypic hippocampal cultures
2011, Journal of Neuroimmunology1-Methyl-1,2,3,4-tetrahydroisoquinoline and established uncompetitive NMDA receptor antagonists induce tolerance to excitotoxicity
2010, Pharmacological ReportsCitation Excerpt :A more recent study demonstrated an NR2A-mediated CREB phosphorylation and a subsequent expression of neuroprotective genes, including cpg15 [12]. Moreover, in vivo studies demonstrate inhibitory effects of MK-801 on brain ischemic preconditioning [9, 25], although these results have been disputed [19, 58]. In turn, the mechanism of preconditioning with NMDA receptor antagonists has been explained by the effect of mild oxidative stress induced by the transient inactivation of NMDA receptors [53].
Knockdown and overexpression of NR1 modulates NMDA receptor function
2009, Molecular and Cellular Neuroscience