Skip to main content
. 2019 Jul 10;39(28):5424–5439. doi: 10.1523/JNEUROSCI.1341-18.2019

Figure 3.

Figure 3.

Adult loss of both CAMK2A and CAMK2B does not cause alterations of the postsynaptic density. a, b, Western blot examples of synaptosomes, soluble fraction and PSD-enriched fraction probed with common PSD proteins antibodies (PSD95, NR2B, and GluR2) of cortical lysates from Camk2af/f;Camk2bf/f;CAG-CreESR (a, n = 6; b, n = 6) and Camk2af/f;Camk2bf/f control mice (a, n = 6; b, n = 8) killed at 21 d after gene deletion (Group 1; a) or just before death (Group 2; b). Actin was used as a control to show efficient enrichment in the PSD fraction of solely PSD proteins. c, d, Quantification of protein levels in the synaptosomes fraction (top) and in the PSD fraction (bottom). Synaptosomes show equal starting levels for both Camk2af/f;Camk2bf/f;CAG-CreESR and control mice for all PSD proteins. Quantification of the PSD associated fraction of PSD95, NR2B, GluR2 shows no difference between the control mice and Camk2af/f;Camk2bf/f;CAG-CreESR mice at either time points of analysis. Error bars indicate SEM. **p < 0.005; ***p < 0.0001.