Supplementary Figure 2: Amyloid fibrils preferentially attenuated hippocampal glutamatergic transmission.
From: Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency
(a) Amyloid fibrils (Aβ1-40) significantly increased the paired-pulse ratio of evoked EPSC, indicating decreased presynaptic glutamate release in hippocampal neurons (n = 11 and 9 neurons, F(1,18) = 14.1, P = 0.002), and decreased the exogenous AMPA (1 μM)-induced inward currents, indicating attenuated postsynaptic response in hippocampal CA1 neurons (b, n = 11 and 8 neurons, t = 2.5, P = 0.022). Representative traces of mEPSC and mIPSC of hippocampal CA1 neurons in control and amyloid-injected rats were shown (c). Amyloid fibrils significantly decreased the amplitude (d, n = 13 and 17 neurons, t = 2.8, P = 0.009) and frequency (e, n = 13 and 17 neurons, t = 2.4, P = 0.025) of mEPSC, but not mIPSC, in hippocampal CA1 neurons. (f) Amyloid fibrils decreased the mEPSC/mIPSC ratio of amplitude (n = 17 and 19 neurons, t = 2.3, P = 0.03) and frequency (n = 17 and 19 neurons, t = 4.8, P<0.001) in hippocampal CA1 neurons. (g) Immunofluorescence for inhibitory GABAergic presynaptic marker GAD67 (green) and excitatory glutamatergic presynaptic marker vGLUT1 (violet) in the hippocampal CA1 in control and amyloid-injected rats. Note a marked decrease in vGLUT1, but not GAD67, immunoreactivities was observed (n = 25 sections from 5 rats in each group, t = 2.456, P = 0.39, scale bar = 25 μm). Data represent mean ± s.e.m. *, P<0.05, **, P<0.01.
