Fig. 5

Ketamine reversed the enhanced extrasynaptic p-CaMKIIα–GluN2B interaction in the hippocampus induced by LPS. a Immunoprecipitation of GluN2B with p-CaMKIIα and CaMKIIβ in extrasynaptic fractions of the hippocampus. b Ketamine administration attenuated the enhanced interaction between p-CaMKIIα and GluN2B induced by LPS. c The levels of CaMKIIα and GluN2B in the DIV11 hippocampal neurons after transfection with control siRNA and CaMKIIα siRNA were determined by western blotting. d CaMKIIα siRNA decreased GluN2B level in the hippocampal neurons. e CaMKIIα siRNA decreased CaMKIIα level in the hippocampal neurons. f DIV10 hippocampal neurons were transfected with control siRNA and CaMKIIα siRNA, fixed on DIV11, and immunostained with antibodies to CaMKIIα. Shown are representative confocal images of transfected neurons. g CaMKIIα siRNA decreased the mean intensity of CaMKIIα signals in the cell body and dendrites in f. h DIV10 hippocampal neurons were transfected with control siRNA and CaMKIIα siRNA, fixed on DIV11, and immunostained with antibodies to GluN2B. Shown are representative confocal images of transfected neurons. i CaMKIIα siRNA decreased the mean intensity of GluN2B signals in the cell body and dendrite and the GluN2B puncta per 100 μm dendrite length in (h). Scale bars indicate 20 μm. Data are presented as mean ± SEM (n = 4–6 mice per group or n = 60 neurons). *p < 0.05 vs the Sal + Sal group; ^##p < 0.01 vs the LPS + Sal group; ^&p < 0.05, ^&&&&p < 0.0001 vs the control siRNA group