Fig. 2

Impairment of ER Ca²⁺ homeostasis in lateral and medial perforant pathways of PS cDKO mice. a and d Depicted images of DG area show that the stimulation (Sti) and recording pipette (Rec) are positioned at the LPP or MPP, respectively. b Representative EPSCs evoked by 6 repetitive LPP stimuli at 20 Hz recorded before and after addition of the SERCA inhibitor, TG (2 μM for 30 min). The evoked EPSCs were elicited with 100 µA stimulation intensity by the stimulation electrode placed at LPP and recorded at a holding potential of −80 mV in whole-cell configuration. Summary graphs show that the frequency facilitation of evoked EPSCs is decreased in PS cDKO neurons relative to slices from control mice (p = 0.0025; two-way ANOVA). The TG treatment of slices from control mice results in reduced frequency facilitation of EPSC amplitudes (p = 0.04; two-way ANOVA), whereas TG treatment of slices from PS cDKO mice fails to reduce the magnitude of frequency facilitation triggered by stimulus trains (p = 0.75; two-way ANOVA). c Summary graphs display the sum of EPSC amplitudes before and after TG application at LPP. e Representative EPSCs evoked by 6 repetitive MPP stimuli at 20 Hz recorded before and after addition of TG. Frequency depression of evoked EPSCs elicited by the MPP stimulation becomes more pronounced in slices from PS cDKO mice (p = 0.0012, two-way ANOVA). The TG treatment of slices from control mice results in enhanced frequency depression (p = 0.04, two-way ANOVA), whereas TG treatment of slices from PS cDKO mice fails to further enhance frequency depression (p = 0.14; two-way ANOVA). f Summary graphs display the sum of EPSC amplitudes before and after TG application at MPP. All data represent mean ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001; NS: not significant). The number of neurons/mice used in each experiment is shown in parentheses