Fig. 2
From: Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway
Phf8 null mice display compromised long-term potentiation and enhanced basal synaptic transmission. a Shown are the slopes of field excitatory postsynaptic potentials (fEPSP) before and after tetanic stimulation (a train of 100 Hz stimulation for 1 s) recorded from hippocampal slices (WT, n = 7 slices from five mice; KO, n = 8 slices from six mice). Sample traces show averaged baseline responses (black) and responses during the last 10 min of recording (red) in WT and Phf8 KO animals. The ratio between fEPSP during the last 10 min recording and baseline is analyzed to evaluate the potentiation (right panel, 129.3 ± 5.1% in WT vs. 107.4 ± 6.0% in KO; unpaired two-tailed t-test, p = 0.0164). b Plot of input–output relationship (I–O curve) at Schaffer collateral-CA1 synapses in the hippocampal slices(one-way ANOVA, F(1, 207) = 14.401, p = 0.0002). The I–O curve obtained from PHF8-mutant mice is left-shifted compared with control (WT, n = 10 slices from five mice; KO, n = 9 slices from five mice). c Presynaptic fiber volley amplitude measured at increasing stimulus intensities (10–100 μA, one-way ANOVA, F (1, 207) = 1.000, p = 0.3185). d Scatter plot of fEPSP slope vs. diverse fiber volley amplitudes. The horizontal and vertical bars indicate the standard errors for fiber volley amplitudes and slope of the fEPSP, respectively. e Paired-pulse ratio measured at different inter-stimulus intervals reveals no differences in presynaptic release of transmitter between WT and Phf8 KO groups (n = 10 slices from five mice for each genotype; one-way ANOVA, F (1,138) = 0.444, p = 0.5063). All data are shown as mean ± s.e.m. *p < 0.05
