Fig. 3: Dampened glutamatergic transmission by chronic dexamethasone exposure in cultured neurons and after 4 weeks of CUS exposure in young adult mice.
a Representative whole-cell current traces of AMPAR-mediated mEPSCs recorded from DIV15 control cortical neurons or neurons exposed to dexamethasone (250 nM, DIV7-15). b Long-term exposure to dexamethasone decreased the amplitude of AMPAR-mediated mEPSCs (n = 7 independent experiments, 20–25 cells per condition; Nested t-test: #p ≤ 0.05). c The cumulative probability curve of mEPSC amplitudes of neurons treated with dexamethasone presented a leftward shift (smaller amplitudes; n = 7 independent experiments, 100 events/cell, 20–25 cells per condition). d Representative images of cortical neurons submitted to prolonged GR activation with dexamethasone (250 nM, DIV7-16) or under control conditions and labelled for surface AMPARs (GluA), PSD95, VGluT1 and MAP2. e Chronic dexamethasone treatment decreased the intensity of synaptic AMPARs (n = 3 independent experiments, 30–32 cells per condition; Nested t-test: ns p > 0.05; ##p ≤ 0.01). f Representative whole-cell current traces of AMPAR-mediated mEPSCs recorded from the mPFC of mice after 4 weeks of CUS. g The CUS protocol decreased the amplitude of AMPAR-mediated mEPSCs (n = 3 animals per condition, 18–19 cells per condition; Nested t-test: #p ≤ 0.05). h The cumulative probability curve of mEPSC amplitudes of neurons from CUS animals presented a leftward shift (smaller amplitudes; 3 animals per condition, 50 events/cell, 18–19 cells per condition). i Representative images of layer 5–6 mPFC region from young naïve or CUS mice labelled for GluA2 and VGluT1. j Intensity and k area of GluA2 clusters decreased in the mPFC region of CUS mice (n = 3–4 animals per condition, 8 fields of view/animal). e, j, k Boxes show 25th and 75th percentiles, whiskers show the range (minimum to maximum values) and the horizontal line shows the median value. b, g Results are presented as mean ± SEM.
