Fig. 2
From: Tau oligomers impair memory and synaptic plasticity through the cellular prion protein
TauOs, but not the monomer (TauM), impair memory and synaptic plasticity in WT but not in Prnp0/0 mice. a Scatter plots ± standard error mean (SEM) of the DI of WT mice receiving a single ICV injection of Veh (n = 10), TauM (n = 9) or TauOs (n = 9) and then tested in the NORT; (One-Way ANOVA: F(2,25) = 16.28, P < 0.001); *** P < 0.001, ****P < 0.0001 Tukey’s post-hoc test. b Scatter plot ± SEM of the DI of WT or Prnp0/0 mice treated with Veh (WT: n = 6; Prnp0/0 n = 9) or TauOs (WT: n = 6; Prnp0/0 n = 10) and tested in the NORT. Two-way ANOVA found an effect of: Tg F(1, 27) = 3,481, P = 0.073, Treatment F(1, 27) = 8.32, P = 0.0076 and a significant Interaction F(1, 27) = 11.01, P = 0.0026; * P < 0.05, **P < 0.01, Tukey’s post-hoc test. c Time course of LTP in the CA1 hippocampal area in slices from WT mice pre-incubated for 60–90 min with either Veh (n = 7), 100 nM monomers (n = 7) or 100 nM TauOs (n = 7). Two-way ANOVA for repeated measures found: VEH vs. TauM F(1,12) = 0.18, P = 0.68; VEH vs. TauOs F(1,12) = 14.62, P = 0.002; TauOs versus TauM F(1,12) = 11.45, P = 0.005; (n = 7/group). d Data are scatter plots ± SEM of residual potentiation calculated by averaging the slopes of the field excitatory postsynaptic potentials (fEPSP) in the last 10 min of LTP recorded in WT slices. One-way ANOVA for treatment factor found: F(2,18) = 26.39, P < 0.0001; VEH vs. TauOs P < 0.0001; TauM vs VEH P = 0.51; TauOs vs. TauM P < 0.0001. ***P < 0.001, ****P < 0.0001; Tukey’s post-hoc test). e Time course of LTP in the CA1 hippocampal area in slices from Prnp0/0 mice preincubated with Veh or TauOs. f Scatter plot ± SEM of residual potentiation calculated by averaging the fEPSP slopes in the last 10 min of LTP in Prnp0/0 slices (t9 = 2.26, P = 0.985)