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. 2017 Jun 30;16(5):1062–1072. doi: 10.1111/acel.12634

Figure 2.

Figure 2

Inhibition of G9a/GLP complex activity rescues Aβ‐induced deficits in LTP. (A) Aβ‐treated hippocampal slices expressed late‐LTP in the presence of UNC 0638 (UNC, 150 nm), where drug was bath applied 30 min before and after the LTP induction by STET (filled circles, n = 7). (B) Same experiment as in A, but with another G9a/GLP inhibitor BIX 01294 (BIX, 500 nm, n = 6). The control potentials were stable throughout the recording (open circles). (C‐F) Co‐application of UNC or BIX with protein synthesis inhibitors anisomycin (25 μm) or emetine (20 μm) prevented the rescue of late‐LTP (filled circles) in the hippocampal slices pretreated with Aβ (C, n = 6, D, n = 6, E, n = 9 and F, n = 6). Control potentials were stable in all the cases (open circles). (G‐H) Effect of the NMDA receptor blocker AP‐5 on G9a/GLP inhibition mediated rescue of Aβ‐induced plasticity impairment: STET in the presence of AP‐5 (50 μm) along with either UNC (G, n = 6) or BIX (H, n = 5) prevented the establishment of late‐LTP (filled circles); the control recording of S2 remained stable during the recorded period (open circles). Error bars indicate ± SEM. Symbols and analog traces as in Fig. 1.