Fig. 7
Loss of γ2 AMPK increases resting heart rate and SA cell automaticity. a Cardiac western blot for γ AMPK isoforms in Sox2cre-driven γ2 knockout mice (Homo fl Cre+) and WT Sox2cre carrying controls (WT Cre+). b HR of Homo fl Cre+ and WT Cre+ mice under anesthesia (n = 7–12). c HR during ex vivo-isolated cardiac perfusion (n = 8–9). d Representative action potentials recorded from isolated SA cells. e Mean beating rate of SA cells from genotypes illustrated in d (n = 18–20 cells/3–5 mice). f, g Relative gene expression (by qRT-PCR) of Hcn1 and Hcn4 from whole hearts (n = 5–6). h Representative I f traces during steps to −125 mV. (i) Mean I f density at −125 mV (n = 28–31 cells/7–8 mice). j Mean voltage dependence of I f activation of isolated SA cells (n = 7–9). Uncropped western blots are shown in Supplementary Fig. 10. b, c, e–g, i Student’s t-test was performed. *P < 0.05, **P < 0.01. b, c, e–g, i Data are shown as means ± s.e.m.
