(A–C) Population spikes were elicited by half-maximal electrical stimulation at 0.03 Hz (indicated by arrow). Insets in (A), (B), and (C) are averaged traces recorded before applying a very low concentration of bicuculline (2 µM), which generated pronounced after-discharges in Pkr−/− slices (B) or WT slices treated with PKRi (1 µM) (C), but not in WT slices (A). For all plots, n ≥ 5; calibrations: 2 ms and 3 mV for insets and 10 ms and 5 mV for slow traces.
(D and E) Compared to WT slices, the number of evoked spikes (D, F(2, 24) = 66.3; **p < 0.01) and the duration of burst (E, F(2.24) = 100.2; **p < 0.01) were increased in Pkr−/− slices or WT slices treated with PKRi.
(F–K) Similar intrinsic neuronal properties and basal synaptic transmission but maximal fEPSPs elicited larger population spikes in Pkr−/− slices.
(F) Input-output data show similar amplitudes of presynaptic fiber volleys over a wide range of stimulus intensities in WT and Pkr−/− slices. Mean afferent volley versus stimulus strength were fitted by linear regression (R2 = 0.989 for WT and 0.993 for Pkr−/− slices).
(G) fEPSPs as a function of presynaptic fiber volley did not differ between WT and Pkr−/− slices (linear regression; R2 = 0.643 for WT and 0.638 for Pkr−/− slices).
(H) Paired-pulse facilitation of fEPSPs did not differ between WT and Pkr−/− slices, as shown by the plots of the PP ratio (fEPSP2/fEPSP1) for various intervals of paired stimulation.
(I) Sigmoidal relationship of population spikes versus fEPSP, though initially similar, reached a higher ceiling in Pkr−/− slices.
(J and K) In whole-cell recordings in the presence of glutamate and GABA antagonists, resting membrane potential was −59 ± 1.23 mV for WT and −60 ± 1.22 mV for Pkr−/− slices (p > 0.05), and input resistance was 397 ± 24 MΩ for WT and 381 ± 39 MΩ for Pkr−/− slices (p > 0.05). Inward and outward current pulses generated similar voltages changes (J) and numbers of spikes (K) in WT and Pkr−/− slices.
For information about the effect of PKRi in vitro, see Figure S7C.