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. 2016 Oct 19;9:102. doi: 10.3389/fnmol.2016.00102

Figure 5.

Figure 5

Glycine increases ERK1/2 phosphorylation through metabotropic activity of GluN2ARs in HEK293 cells. (A) The levels of ERK1/2 phosphorylation are not altered by glycine (100 μM) treatment in non-transfected HEK293 cells where NMDARs and glycine receptors are inhibited (n = 6). (B) In HEK293 cells transfected with GluN1+GluN2A cDNAs, the ERK1/2 phosphorylation is increased by glycine (100 μM) treatment after NMDARs and glycine receptors are inhibited (n = 6, *p < 0.05). (C) In HEK293 cells transfected with GluN1 + GluN2A + GluN2B cDNAs, the ERK1/2 phosphorylation is increased by glycine (100 μM) treatment after NMDARs and glycine receptors are inhibited (n = 6, *p < 0.05). (D) In HEK293 cells transfected with GluN1 + GluN2B cDNAs, the levels of ERK1/2 phosphorylation are not altered by glycine (100 μM) treatment after NMDARs and glycine receptors are inhibited (n = 6). (E) In HEK293 cells transfected with cDNAs of GluN1, GluN2A or GluN2B, respectively, the levels of ERK1/2 phosphorylation are not altered by glycine (100 μM) treatment after NMDARs and glycine receptors are inhibited (n = 6). (F) In HEK293 cells transfected with GluN1(N598Q) + GluN2A, glycine enhances Erk phosphorylation (n = 6, *P < 0.05 vs. -Gly). Con: Control; Gly: glycine.