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. 2013 May 14;6:24. doi: 10.1186/1756-6606-6-24

Figure 2.

Figure 2

5-CT treatment of hippocampal slices increases NR1 phosphorylation at serines 896 and 897. A) Hippocampal slices were treated with 50 nM 5-CT in the absence or presence of 1 (micro)M Go 6983 (GO) for 5 min. Increases in the phosphorylation state at serine 896 were normalized to control (vehicle-treated slices) and to total NR1. Data represent the average and standard error of 10 independent experiments. * p < 0.5 compared to vehicle, ANOVA analysis with Dunnett’s post-test. INSET: representative Western blots showing serine 896 phosphoryaltion and the β-actin loading control. B) Hippocampal slices were treated with 50 nM 5-CT in the absence or presence of 10 μM H89 for 5 min. Data represent the average and standard error of 10 independent experiments. * p < 0.5 compared to vehicle, ANOVA analysis with Dunnett’s post-test. INSET: representative Western blots showing serine 897 phosphoryaltion and the β-actin loading control. C) Hippocampal slices were treated with 50 nM 5-CT or 300 nM LP 12 for 5 min, the slices were washed and incubated in drug-free buffer for an additional 20 min before lysis. Data represent the average and standard error of 8 independent experiments. * p < 0.5 compared to vehicle, ANOVA analysis with Dunnett’s post-test. INSET: representative Western blots showing serine 896 phosphoryaltion and the β-actin loading control. D) Slices were treated as in C. Data represent the average and standard error of 4 independent experiments. * p < 0.5 compared to vehicle, ANOVA analysis with Dunnett’s post-test. INSET: representative Western blots showing serine 897 phosphoryaltion and the β-actin loading control.