Fig. 4: Brain regional specific effects of tau on Aβ-induced synaptic plasticity impairments. | Molecular Psychiatry

Fig. 4: Brain regional specific effects of tau on Aβ-induced synaptic plasticity impairments.

From: Synaptic vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits

Fig. 4

A, F Input-output curves showing EPSC amplitudes (A) and fEPSP slope (F) vs the applied stimulus intensity in CA3/CA1 hippocampal (A) and thalamus-lateral amygdala (LA) (F) synapses of control (WT, white), APP (red), Tau (blue), and APP/Tau (grey) mice. B, G Traces (top) and time course (bottom) of fEPSPs before and after LTP induction in CA3-CA1 hippocampal (B) and thalamus-LA synapses (G). C, H Histograms showing short-term synaptic plasticity (STP), early long-term potentiation (E-LTP), late LTP (L-LTP) in CA3-CA1 hippocampal (C) and thalamus-LA synapses (H). D, I Paired-pulse facilitation (PPF) does not change after LTP induction in the hippocampus (D) or amygdala (I), and baseline PPFs of APP are decreased in the hippocampus and amygdala compared to controls. However, PPF of APP/Tau mice is significantly decreased only in hippocampus. E, J NMDA/AMPA ratio was decreased in hippocampal neurons of APP/Tau mice compared to control, APP, and Tau mice (E). In amygdala (J), NMDA/AMPA ratio was not affected in the transgenic mice. Data represent mean ± SEM from electrophysiological recordings in CA3-CA1 and thalamic-LA synapses of 6 month-old female control (n = 7–8), APP (n = 5–6), Tau (n = 7–8), and APP/Tau (n = 6) mice. Statistical analysis was determined by one-way ANOVA or Kruskal-Wallis tests according to the D’Agostino-Pearson omnibus normality test, followed by Tukey’s or Dunn’s post hoc test, respectively (D, E, I, J) or two-way ANOVA (A, F) followed by Tukey’s post-hoc test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs the indicated group.

Back to article page