Fig. 5

Hippocampal depotentiation is enhanced in THY-tau22 transgenic mice. (a) DP was significantly stronger in 12-month-old THY-tau22 transgenic mice (TG, n = 8) compared to THY-tau22 wild-type littermates (WT, n = 8) (F _{(1, 14)} = 5.235, *p = 0.038), while no significant differences were observed in basal synaptic transmission (inset; p = 0.859) or the initial fEPSP potentiation after TBS (p = 0.482). This abnormal enhancement of DP in THY-tau22 TG could not be rescued by bath-application of the GSK3β inhibitor SB216763 (10 μM, n = 6), since a significant difference between treated slices and WT controls was still evident (F _{(1, 12)} = 8.21, *p = 0.014). Arrow represents single TBS, open square TPS, and open rectangle drug application. Error bars indicate SEM. Traces show representative examples of field excitatory postsynaptic potentials (fEPSP) recorded during baseline, 1 min post-TBS delivery (IP 1 min), 1 min post-TPS delivery (DP 1 min), and 120 min post-TPS delivery (DP 120 min). Calibration bars: 0.5 mV and 5 ms. Curve-fitting of DP data extended the results of RM-ANOVAs. Mean values for τ _rise (b) were statistically similar between slices from transgenic mice (TG or TG + SB216763) and their wild-type littermates (WT). In contrast, mean ‘plateau levels’ (c) were significantly lower in THY-tau22 TG or THY-tau22 TG + SB216763 compared to THY-tau22 WT (TG × WT: t (12.6) = 2.752, *p = 0.017; TG + SB216763 × WT: t (10.9) = 3.113, **p = 0.010)