Fig. 5: MiR-186-5p inhibition rescued the dexamethasone-induced deficits in excitatory synapses.
a Representative images of DIV16 cortical neurons expressing either a miR-186-5p inhibitor or a scramble sequence, under control conditions or exposed to dexamethasone (250 nM, DIV7-16). Neurons were labelled for surface AMPARs (GluA), VGluT1 and MAP2. b MiR-186-5p inhibition rescued the intensity of synaptic GluA clusters in dexamethasone treated neurons to control levels (n = 4 independent experiments, 45–48 cells per condition; Nested One-way ANOVA: p = 0.0041, followed by Tukey’s multiple comparisons test: ns p > 0.05; ##p ≤ 0.001). c Representative whole-cell current traces of AMPAR-mediated mEPSCs recorded from DIV15 cortical neurons expressing a scramble sequence or a miR-186-5p inhibitor, under control conditions or treated with dexamethasone (250 nM, DIV7-15). d Amplitudes of mEPSCs of neurons expressing the miR-186-5p inhibitor under chronic GR activation are not different from those of scramble-expressing neurons under control conditions (n = 5 independent experiments, 18–21 cells per condition; Nested One-way ANOVA: p = 0.0267, followed by Tukey’s multiple comparisons test: #p ≤ 0.05). e The cumulative probability curve of mEPSC amplitudes of scramble-expressing neurons treated with dexamethasone presented a leftward shift (smaller amplitudes) in comparison with control scramble-expressing neurons; this was prevented by miR-186-5p inhibition (n = 5 independent experiments, 100 events/cell, 18–21 cells per condition). b Boxes show 25th and 75th percentiles, whiskers show the range (minimum to maximum values) and the horizontal line shows the median value. d Results are presented as mean ± SEM.
