Skip to main content
Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models

Fig. 4

Hippocampal depotentiation is unaltered in APPPS1–21 transgenic mice. (a) DP was normal in 14-month-old APPPS1–21 transgenic mice (TG, n = 9) compared to APPPS1–21 wild-type littermates (WT, n = 9) (p = 0.901). Likewise, there were also no significant differences in basal synaptic transmission (inset; p = 0.165) or initial fEPSP potentiation after TBS (p = 0.946). Bath-application of the GSK3 inhibitor SB216763 (10 μM, n = 5) in a subset of APPPS1–21 TG slices did not alter their DP profiles (p = 0.507). Arrow represents single TBS, open square represents TPS, open rectangle represents drug application. Error bars represent 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 confirms the results of RM-ANOVAs. Mean values for τ rise (b) were statistically similar between slices from APPPS1–21 TG, APPPS1–21 TG + SB216763 and their wild-type littermates (APPPS1–21 WT). Likewise, mean ‘plateau levels’ (c) were statistically indistinguishable between genotypes or conditioning groups

Back to article page