Active Calcium/Calmodulin-Dependent Protein Kinase II (CaMKII) Regulates NMDA Receptor Mediated Postischemic Long-Term Potentiation (i-LTP) by Promoting the Interaction between CaMKII and NMDA Receptors in Ischemia

Figure 5

(a) Co-IP assay with anti-CaMKII antibody revealed the association of CaMKII and NMDAR. Peptides occluded the increase of CaMKII and NDMAR by OGD treatment while scramble peptides showed no effect. Arrowhead indicates the nonimmune IgG heavy chain. (b) One hour after photothrombosis caused an increase in the interaction between CaMKII and NMDAR. Arrowhead indicates the nonimmune IgG heavy chain. ((c)-(d)) Peptides Tat-GluN2B suppressed the autophosphorylation of CaMKII in OGD model, compared with control, 1.01±0.04, 𝑛=4, 𝑃>0.05, while scramble peptides failed to exert any effect on OGD model, compared with control, 1.11±0.03, 𝑛=4, ^∗𝑃<0.05. (e) Peptides Tat-GluN2B decreased the CaMKII relative activity when 10 min OGD was applied, compared with control, 0.97±0.04, 𝑛=4, 𝑃>0.05, while scramble peptides failed to exert any effect when 10 min OGD was used, compared with control, 1.66±0.18, 𝑛=4, ^∗𝑃<0.05. (f) Peptides Tat-GluN2B led to impaired i-LTP when the hippocampal slice was exposed to OGD for 10 min, 𝑛=5, compared with OGD, 𝑛=3, 0.73±0.02, 𝑃<0.05. Scramble peptides were used when the hippocampal slice was exposed to OGD for 10 min, 𝑛=5, compared with OGD, 1.02±0.03, 𝑃>0.05. As a control, OGD treatment for 10 min exhibited normal i-LTP. Overlaid traces above the graph showed changes in amplitude of fEPSPs chosen at the times indicated on the graph.

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