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Fig. 2 | Molecular Brain

Fig. 2

From: Inactivation of Presenilin in inhibitory neurons results in decreased GABAergic responses and enhanced synaptic plasticity

Fig. 2

Reduced feed-forward inhibition in hippocampal CA1 neurons of IN-PS cDKO mice. a Schematic drawing shows the circuitry for bi-phasic synaptic responses in CA1 pyramidal neurons triggered by the SC stimulation. b Representative bi-phasic synaptic responses in CA1 pyramidal neurons. Bi-phasic responses were obtained by placing the stimulation electrode away from the recording electrode in the CA1 stratum pyramidale, and IPSCs were recorded at a holding potential of 0 mV and EPSCs were recorded at a holding potential of − 75 mV with low [Cl] Cs+-based pipette solution. Synaptic currents recorded at 0 mV were completely blocked by GABAA receptor antagonist bicuculline (20 µM, Bic; green trace at 0 mV). However, the peak amplitude of synaptic currents at − 75 mV was not affected by bicuculline (green trace at − 75 mV). c Both IPSC and EPSC (recorded at 0 mV and − 75 mV, respectively) were blocked by NBQX (10 µM) and AP5 (50 µM) (orange traces at 0 mV or − 75 mV). d Evoked feed-forward di-synaptic IPSCs in slices from control and IN-PS cDKO mice at different stimulation intensities. IN-PS cDKO neurons show reduction of evoked IPSC amplitudes (F1, 21 = 18.58, p = 0.0003, two-way ANOVA). e Normal input/output relations for evoked glutamatergic EPSCs obtained from SC stimulation in slices from control and IN-PS cDKO mice (F1, 21 = 0.05, p = 0.83, two-way ANOVA). f Summary plot showing the averaged EPSC/IPSC amplitude ratios in CA1 pyramidal neurons. IN-PS cDKO neurons exhibit significant increases of the EPSC/IPSC ratio compared to controls (F1, 21 = 12.93, p = 0.002, two-way ANOVA). All data represent mean ± SEM (** p < 0.01, *** p < 0.001). The number of neurons/mice used in each experiment is shown in parentheses

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