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. 2019 Jan 22;142(3):787–807. doi: 10.1093/brain/awy354

Figure 4.

Figure 4

AMPAR- and NMDAR-mediated synaptic transmission was significantly diminished in FAD mice, which was restored by EHMT1/2 inhibitors. (A and B) Input-output curves (mean ± SEM) of AMPAR-EPSC (A) and NMDAR-EPSC (B) in response to a series of stimulation intensities in PFC pyramidal neurons from wild-type and FAD mice (5–6 months old) treated with BIX01294 (1 mg/kg, s.c. 3×) or saline control. **P < 0.01, ***P < 0.001, two-way rmANOVA. Bottom: Representative EPSC traces at different stimuli. (C) Paired-pulse ratio (PPR) of AMPAR-EPSC in PFC pyramidal neurons of wild-type (WT) versus FAD mice. Bottom: Representative traces of AMPAR-EPSC evoked by paired pulses at different intervals. (D) Bar graphs showing coefficient of variations (CV) of AMPAR-EPSC in PFC pyramidal neurons of wild-type versus FAD mice. (E and F) Input-output curves (mean ± SEM) of AMPAR-EPSC (E) and NMDAR-EPSC (F) in response to a series of stimulation intensities in PFC pyramidal neurons from wild-type and FAD mice (5–6 months old) treated with the EHMT1/2 inhibitor UNC0642 (1 mg/kg, i.p. 3×) or saline control. *P < 0.05, **P < 0.01, ***P < 0.001, two-way rmANOVA. (G) I-V curves of calcium currents through voltage-dependent calcium channels (VDCCs) in PFC pyramidal neurons from wild-type versus FAD mice. (H) Representative VDCC current traces. Each set of the experiments was replicated between four and six times.