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. 2018 Mar 12;115(13):E3007–E3016. doi: 10.1073/pnas.1718883115

Fig. 4.

Fig. 4.

Scopolamine reduces sIPSC frequency and amplitude, increases sEPSC amplitude, and disinhibits CA1 pyramidal cells. (A) Representative traces showing scopolamine decreases sIPSC frequency and peak amplitude compared with baseline. (Scale bars: 100 pA and 5 s; Inset, 100 pA and 500 ms.) (B) Cumulative probability showing a significant increase in the sIPSC IEI in the presence of scopolamine (P < 0.05, n = 7, 2,700 baseline events, 2,500 scopolamine events) and a decrease in sIPSC peak amplitude (P < 0.0001, n = 7, 2,700 baseline events, 2,500 scopolamine events). (C) Representative traces from baseline conditions and in the presence of scopolamine. (Scale bars: 20 pA and 3 s; Inset, 20 pA and 500 ms.) (D) Cumulative probability showing no change in sEPSC IEI (P = 0.29, n = 5, 1,300 baseline events, 1,300 scopolamine events) and increased peak amplitude with bath application of scopolamine (P < 0.0001, n = 5, 1,300 baseline events, 1,300 scopolamine events). (E) Schematic of whole-cell recordings of CA1 pyramidal cells showing the effects of scopolamine on intrinsically (1) and synaptically (2) driven APs. (Scale bars: 20 mV and 100 ms.) (Inset) Representative subthreshold EPSP-IPSP traces from cell 12 in the raster plot; compared with the baseline trace (black), scopolamine decreases the IPSP magnitude (red trace, black arrow). (Scale bars: 2 mV and 50 ms.) (F) Raster plot and summary plots showing a significant increase in synaptic AP probability in the presence of scopolamine (*P < 0.05, n = 13). (G) No change in the measured intrinsic properties (Direct AP number, AP threshold, and input resistance) is observed (n = 13). (Scale bars: 20 mV and 100 ms, 4 mV and 100 ms.) All values are mean ± SEM.