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. 2020 May 6;40(19):3741–3750. doi: 10.1523/JNEUROSCI.0046-20.2020

Figure 7.

Figure 7.

CaMKII activity is required for spine shrinkage driven by non-ionotropic NMDAR signaling. A, Images of dendrites from CA1 neurons of acute slices from P16 to P20 GFP-M mice before and after HFU (yellow cross) at single spines (yellow arrowhead) in the presence of L-689, L-689 with 10 μm KN-62, or L-689 with 5 μm TAT-CN21. B, C, Inhibition of CaMKII activity with KN-62 (red filled circles/bar; 9 spines/9 cells) or TAT-CN21 (gray filled circles/bar; 9 spines/9 cells) blocked spine shrinkage induced by HFU in the presence of L-689 (black filled circles/bar; 8 spines/8 cells). Volume of unstimulated neighboring spines (open bars) was not changed. *p < 0.05, ***p < 0.001, paired two-tailed t test compared with baseline and calculated across cells. D, Proposed model for the non-ionotropic NMDAR signaling pathway that drives spine shrinkage. Glutamate binding to the NMDAR induces conformational changes that drive dendritic spine shrinkage through NOS1AP–nNOS interactions, and the activities of nNOS, p38 MAPK, MK2, CaMKII, and cofilin-dependent severing of the actin cytoskeleton.