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. 2015 Mar 26;5:9493. doi: 10.1038/srep09493

Figure 1. The effects of nicotine on γ oscillations.

Figure 1

(A1–C1) KA-induced γ oscillation. (A1): Representative traces of extracellular recordings in hippocampal CA3 before and after KA application; The 1-second waveforms were taken from the steady states before and after application of KA. (B1): The power spectra of the field potentials before and after application of KA; (C1): The time course shows the changes of γ power before and after application of KA. (A2–A5) Representative extracellular recordings of field potentials before and after application of nicotine at 0.25 μM (A2), 1 μM (A3), 10 μM (A4) and 100 μM (A5). (B2–B5) Power spectra of field potentials before and after application of nicotine at 0.25 μM (B2), 1 μM (B3), 10 μM (B4) and 100 μM (B5); (C2–C5) The time courses showing the changes of γ power before and after application of nicotine at 0.25 μM (C2); 1 μM (C3), 10 μM (C4) and 100 μM (C5). (D): Bar graph summarizes the percent changes in γ power before and after application of various concentrations of nicotine. Gray bar: Normalized γ power in control (100%, KA alone). Black bars: The percent changes in γ powers after application of various concentrations of nicotine. *p < 0.05, **p < 0.01, ***p < 0.001, compared with control, one way RM ANOVA, n = 9, 13, 10, 10 for 0.25 μM, 1 μM, 10 μM and 100 μM nicotine, respectively. (E): Bar graph summarizes the changes in peak frequency of γ oscillations before and after application of various concentrations of nicotine. Gray bars: Control peak frequency (KA alone), Black bars: The peak frequency after application of various concentrations of nicotine (*p < 0.05, **p < 0.01, compared with control, one way RM ANOVA).