Fig. 4
From: Presenilins regulate synaptic plasticity in the perforant pathways of the hippocampus
Impaired LTP and NMDA receptor activation in LPP and MPP of PS cDKO mice. a and e Impaired LTP induced by 5 TBS in LPP and MPP of PS cDKO mice. Superimposed traces are averages of four consecutive responses 7 min and 60 min after (1, 2) TBS induction. b and f Normal AMPAR-mediated input/output curves in both lateral (Control: y = 1.63x, R2 = 0.90; PS cDKO: y = 1.46x, R2 = 0.88) and medial (Control: y = 2.86x, R2 = 0.83; PS cDKO: y = 2.29x, R2 = 0.63) perforant pathway of PS cDKO mice at 2 months of age. The lines represent the best linear regression fit. The input/output slopes are similar between control and PS cDKO mice (LPP: p = 0.22; MPP: p = 0.11; linear regression). c and g The sample traces of evoked AMPAR- and NMDAR-mediated EPSCs recorded in whole-cell voltage clamp mode in the same cell at −80 mV (lower traces) and +40 mV (upper traces) in the presence of Bicuculline, respectively, are shown. The NMDAR-mediated component of the EPSC was measured 50 ms after the peak of the AMPAR EPSCs (marked with blue arrow heads). d and h Summary graphs from left to right show AMPAR- or NMDAR-mediated EPSC amplitudes and NMDAR/AMPAR ratios. Note that the NMDAR/AMPAR ratio is reduced in both LPP and MPP of PS cDKO neurons (LPP: Control: 0.49 ± 0.04, PS cDKO: 0.26 ± 0.03, p < 0.0001; MPP: Control: 0.41 ± 0.03, PS cDKO: 0.32 ± 0.03, p = 0.028; unpaired t-test). All data represent means ± SEM (*p < 0.05, **p < 0.01, ****p < 0.0001). The number of slices or neurons/mice used in each experiment is shown in parentheses