Fig. 4: PSD-95 Phosphorylation at T19 position is essential for all the NMDAR-dependent molecular reshuffling induced by LTD. | Nature Communications

Fig. 4: PSD-95 Phosphorylation at T19 position is essential for all the NMDAR-dependent molecular reshuffling induced by LTD.

From: NMDAR-dependent long-term depression is associated with increased short term plasticity through autophagy mediated loss of PSD-95

Fig. 4

A and B Expression of T19A phospho-null mutant of PSD-95, but not WT PSD-95, suppresses the decrease of GluA2 containing AMPAR (A) and PSD-95 (B) content per nanodomain 30 min following NMDAR-dependent LTD (at left: example of super-resolution intensity images of a piece of dendrite obtained using dSTORM technique). At right, the mean per cell histogram (mean ± SEM, one-way ANOVA, p < 0.0001 and p = 0.0014 respectively and Tukey’s post-test results are realized between each conditions, N = 141, 76, 110, 65, 139, 91 for the measure of AMPAR per nanodomain, and N = 65, 54, 70, 51 for the measure of PSD-95 per cluster). C mEPSC amplitude is significantly decreased 30 min following NMDA treatment when both GFP or WT PSD-95 are expressed, while it is suppressed by T19A PSD-95 expression (mean ± SEM, one-way ANOVA, p < 0.0001 and Tukey’s post-test results are realized between each conditions, N = 18, 12, 10, 8, 21, 18). D Example of trajectories of GluA2-containing receptors with uPAINT technique (left panel) and average distribution of the log(D) (middle panel) when WT (green lines) and T19A (blue lines) mutant PSD-95 are expressed, before (dark lines) and 30 min after (light lines) NMDA treatment. Average of the mobile fraction (Right panel), before and 30 min after NMDA treatment (mean ± SEM, one-way ANOVA, p = 0.009 and Tukey’s post-test results are realized between each conditions, N = 7, 9, 7, 8). WT PSD-95 expressing neurons display an increase of AMPAR mobility following NMDAR-dependent LTD while T19A mutant expression abolished this mobility increase.

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