Fig. 3
From: Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models
Hippocampal depotentiation depends on NMDAR activation. Application of the NMDAR antagonist D-AP5 (50 μM, n = 6) before DP induction resulted in residual fEPSP potentiation being significantly higher than in DP controls (n = 7) (F (1, 11) = 4.945, *p = 0.048). Compared to LTP controls (n = 10), the main conditioning effect of DP 8 was clearly signficant (F (1, 15) = 16.5, **p = 0.001), while this was not the case for slices bathed in D-AP5 (p = 0.3104). 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