Figure 1.

Increased I/E ratio in PGC-1α^−/− mice is caused by enhanced inhibition. A, The I/E ratio in CA1 pyramidal cells, as determined from the peaks of the compound PSC in response to Schaffer collateral stimulation, is greatly enhanced in slices from PGC-1α^−/− mice (n = 10, 6). Inset, Example traces of compound PSCs in CA1 pyramidal cells held at −45 mV from PGC-1α^+/+ (black) and PGC-1α^−/− (red) mice. Scale bars, 50 ms, 50 pA. B, The excitation window (width of the excitatory component of the compound PSC at the points that it crosses 0 pA as depicted by arrows; Chittajallu et al., 2013; Bartley and Dobrunz, 2015) is shorter in slices from PGC-1α^−/− mice. Inset, Example traces of compound PSCs in CA1 pyramidal cells held at −45 mV from PGC-1α^+/+ (black) and PGC-1α^−/− (red) mice. Scale bars, 10 ms, 50 pA. C, The peak amplitude of disynaptic inhibition is enhanced nearly two-fold in slices from PGC-1α^−/− mice (n = 17, 22). Inset, Example traces of disynaptic IPSCs onto CA1 pyramidal cells held at the reversal potential of excitation (0 mV) from PGC-1α^+/+ (black) and PGC-1α^−/− (red) mice. Scale bars, 50 ms, 200 pA. D, The peak amplitude of the EPSCs is not significantly reduced in slices from PGC-1α^−/− mice (n = 12, 13). Inset, Example traces of EPSCs onto CA1 pyramidal cells held at the reversal potential of inhibition (−55 mV) from PGC-1α^+/+ (black) and PGC-1α^−/− (red) mice. Scale bars, 25 ms, 75 pA. E, Input/output curve for disynaptic IPSCs onto CA1 pyramidal cells held at 0 mV indicates that the peak IPSC amplitude is larger in slices from PGC-1α^−/− mice at all stimulation amplitudes above threshold (ANOVA, F_{(7, 40)} = 5.81, p < 0.001, n = 4, 4). F, Input/output curve for EPSCs onto CA1 pyramidal cells held at −55 mV in indicates that the peak EPSC amplitude is not different in slices from PGC-1α^−/− mice across a range of stimulus intensities (ANOVA, F_{(6, 35)} = 1.12, p = 0.37, n = 4, 3). *p < 0.05, Student's t test.