Fig. 7: SLAMR regulates transient structural spine plasticity and basal CaMKIIα activity in CA1 pyramidal neurons. | Nature Communications

Fig. 7: SLAMR regulates transient structural spine plasticity and basal CaMKIIα activity in CA1 pyramidal neurons.

From: Synaptically-targeted long non-coding RNA SLAMR promotes structural plasticity by increasing translation and CaMKII activity

Fig. 7

A Timelapse fluorescence lifetime imaging of a CaMKIIα FLIM-FRET sensor in dendrites of CA1 pyramidal neurons co-expressing SLAMR shRNA-mCherry (TET-SLAMR) or scrambled shRNA-mCherry (NC-mCherry). CaMKIIα is locally activated by a single spine glutamate uncaging (30 pulses, 0.5 Hz). Scale bar = 2 μm. B, C Mean time courses of glutamate uncaging-induced volume change (B) and fluorescence lifetime of a CaMKIIα FLIM-FRET sensor (C) in stimulated dendritic spines expressing NC-mCherry (n = 15 spines/5 neurons) or TET-SLAMR (n = 17 spines/5 neurons). Data are presented as mean ± SEM. D–F Quantifications of volume change (D), basal lifetime of CaMKIIα before glutamate uncaging (E), and glutamate uncaging-induced lifetime change of CaMKIIα sensor (F) (NC-mCherry n = 15 spines/5 neurons, TET-SLAMR n = 17 spines/5 neurons; Two-tailed Mann-Whitney U-test (D–E) Two-tailed unpaired Student’s t-test (F); the data are presented as mean ± SEM). G Schematic of CaMKII in vitro activation assay. H CaMKII activation quantified by Normalized A450 Absorbance values. Normalized by blank subtraction (0 ng/mL Calmodulin, No Template Control (NTC) absorbance value), (N = 4 biological replicates per group, Two-way ANOVA + Tukey’s test; data are presented as mean ± SEM).

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