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. 2023 Jul 26;43(30):5432–5447. doi: 10.1523/JNEUROSCI.0208-22.2023

Figure 7.

Figure 7.

Acute but not long-lasting PKCδ kinase activity is required during plasticity of spines. A, In vitro kinase activity of PKCδ and PKCδ with an inert ATP binding pocket mutation (PKCδ-AS) to varying concentrations of the ATP analog 1NM-PP1. B, Time course and quantification of sLTP in PKCδ WT neurons in the presence of vehicle and 1NM-PP1 (n spines/neurons > 5/5, ns). C, Representative images of sLTP in neurons expressing PKCδ with an inert ATP binding pocket mutation (PKCδ-AS) in place of PKCδ. sLTP was induced in the presence of vehicle or the ATP analog (1NM-PP1, 1 μm) to inhibit PKCδ kinase activity. White dot indicates the location of uncaging. Scale bar, 1 μm. D, Averaged time course of induced volume change of stimulated spines in the presence of vehicle (n = 7) or 1NM-PP1 applied 10 min before (−10 min, n = 11) or 10 min after (+10 min, n = 10) uncaging stimulation. Gray shading represents the time of quantification in E. E, Quantification of mean volume change. One-way ANOVA (F(2,25) = 8.688). **p < 0.0089 (Sidak's multiple comparison post-test), ns, p = 0.999.