Fig. 6

Inhibition of CaMKIIα by KN93 prevented the depression-like behaviors and reduced the elevated extrasynaptic GluN2B localization and phosphorylation in the hippocampus induced by LPS. a KN93 treatment prevented LPS-induced increase in feeding latency in the NSFT, and the total food consumption was not different among the four groups. b KN93 treatment prevented LPS-induced increase in immobility time in the FST. c KN93 treatment reversed LPS-induced increase in extrasynaptic p-CaMKIIα level in the hippocampus. d KN93 treatment reversed LPS-induced increase in extrasynaptic GluN2B level but did not affect synaptic GluN2B level in the hippocampus. e KN93 treatment reversed LPS-induced increase in extrasynaptic p-GluN2B level but did not affect synaptic p-GluN2B level in the hippocampus. f Immunofluorescent images show the colocalization of PSD95 (red) and surface GluN2B receptor (green) in CA1 regions. Arrow indicates colocalization, and triangle indicates no colocalization. g Immunofluorescent images show the colocalization of PSD95 (red) with p-GluN2B (green) in CA1 regions. Arrow indicates colocalization, and triangle indicates no colocalization. h Pearson’s correlation coefficient of PSD95 and GluN2B was not significantly different among the four groups in CA1, CA3, and DG of the hippocampus. i KN93 treatment reversed LPS-induced increase in GluN2B immunoreactivity in CA1, CA3, and DG of the hippocampus. j 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. k KN93 treatment reversed LPS-induced increase p-GluN2B immunoreactivity in CA1 and DG of the hippocampus. Scale bars indicate 20 μm. Data are presented as mean ± SEM (n = 4–10 mice per group). *p < 0.05, **p < 0.01 vs the Sal + DMSO group; ^#p < 0.05, ^##p < 0.01vs the LPS + DMSO group