Effect of Aβ Oligomers on Neuronal APP Triggers a Vicious Cycle Leading to the Propagation of Synaptic Plasticity Alterations to Healthy Neurons

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Figure 10.
Figure 10.

iAβos perturb spontaneous synaptic activity in cultures of mouse cortical neurons. A, Representative traces of AMPA/NMDA sEPSCs at T0 and T20 in control condition or with iAβos (300 nm). B, Bar graphs (mean ± SEM) showing the T20/T0 ratio of AMPA/kainate sEPSC amplitude and frequency in control condition (white bars; n = 10 neurons, Wilcoxon W = −17(19, −36), p = 0.43, for sEPSC amplitudes; and Wilcoxon W = −2(13, −15), p = 0.93, for sEPSC frequencies) or with iAβos (black bars; n = 11 neurons, Wilcoxon W = 2(34, −32), p = 0.9658, for sEPSC amplitudes; and Wilcoxon W = −18(24, −42), p = 0.46, for sEPSC frequencies). Control versus iAβos for AMPA sEPSCs (Mann–Whitney U = 47(102, 129), p = 0.6047, for sEPSC amplitudes; and Mann–Whitney U = 50 (105, 126), p = 0.7561, for sEPSC frequencies). C, Representative traces of NMDA sEPSCs at T0 and T20 in control condition; with iAβos (300 nm). D, Bar graphs (mean ± SEM) showing the T20/T0 ratio of NMDA sEPSC amplitudes and frequencies in control condition (white bars; n = 13 neurons, Wilcoxon W = −55(18, −73), p = 0.0574, for sEPSC amplitudes; and Wilcoxon W = −21(12, −33), p = 0.2383, for sEPSC frequencies); with iAβos (black bars, n = 9 neurons, WilcoxonW = −45(0, −45), p = 0.0039, for sEPSC amplitudes; and Wilcoxon W = −5(11.5, −16.5), p = 0.7188, for sEPSC frequencies). Control versus iAβos for NMDA sEPSCs (Mann–Whitney U = 6(202, 51), p = 0.0001, for sEPSC amplitudes; and Mann–Whitney U = 54.5(145.5, 107.5), p = 0.8041, for sEPSC frequencies). ***p < 0.001; ##p < 0.01, relative to the T0 recording normalized to 100%.

  1. The Journal of Neuroscience vol. 40 no. 27 5161-5176
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