Fig. 4

Ketamine reversed LPS-induced increase in extrasynaptic GluN2B localization and phosphorylation in the hippocampus. The levels of GluN2B and p-GluN2B in extrasynaptic and synaptic fractions of the hippocampus were determined by western blotting and immunofluorescence. a Ketamine administration reversed LPS-induced increase in extrasynaptic GluN2B level but did not affect synaptic GluN2B level in the hippocampus. b Ketamine administration reversed LPS-induced increase in extrasynaptic p-GluN2B level but did not affect synaptic p-GluN2B level in the hippocampus. c Immunofluorescent images show the colocalization of PSD95 (red) and surface GluN2B receptor (green) in CA1 regions of the hippocampus. Arrow indicates colocalization, and triangle indicates no colocalization. d Immunofluorescent images show the colocalization of PSD95 (red) and p-GluN2B (green) in CA1 regions of the hippocampus. Arrow indicates colocalization, and triangle indicates no colocalization. e Pearson’s correlation coefficient of PSD95 and GluN2B was not significantly different among the four groups in CA1, CA3, and DG of the hippocampus. f Ketamine administration reversed LPS-induced increase in GluN2B immunoreactivity in CA1 and DG of the hippocampus. g Pearson’s correlation coefficient of PSD95 and p-GluN2B was not significantly different among the four groups in CA1, CA3, and DG of the hippocampus. h Ketamine administration reversed LPS-induced increase in p-GluN2B immunoreactivity in CA1 and DG of the hippocampus. Scale bars indicate 20 μm. Data are presented as mean ± SEM (n = 4–6 mice per group). *p < 0.05, **p < 0.01 vs the Sal + Sal group; ^#p < 0.05, ^##p < 0.01 vs the LPS + Sal group