Ant-AIP-2 treatment modulates αCaMKII interaction with NR2B in acute hippocampal slices. A, Proteins from P2 crude membrane fraction purified from control and Ant-AIP-2-treated slices were immunoprecipitated with a polyclonal antibody raised against NR2B subunit of NMDA receptor; Western blot analysis was performed in the immunoprecipitated material with anti-NR2B and anti-αCaMKII monoclonal antibodies. B, Diagram illustrating statistical analysis of Western blotting experiments performed in the P2 fraction obtained from control and Ant-AIP-2 (10 μm, 30 min)-treated hippocampal slices. Same amount of proteins was loaded in each lane. Thirty-minute-Ant-AIP-2 treatment does not affect NR2B and αCaMKII localization in the P2 fraction. C, Diagram illustrating statistical analysis of Western blotting experiments performed on NR2B-immunoprecipitated material. Data are expressed as the ratio αCaMKII/NR2B (^#p < 0.005 Ant-AIP-2 30 min vs control; *p < 0.05 Ant-AIP-2 2 h vs control). D, Western blot analysis of the TIF obtained from control and Ant-AIP-2 (10 μm, 30 min)-treated hippocampal slices. Same amount of proteins were loaded in each lane. Thirty-minute-Ant-AIP-2 treatment does not affect NR2B and αCaMKII localization in the TIF.