Fig. 4 Loss of miR-19b induces prolongation of the action potential
(a) Schematic illustration of an action potential with major depolarizing and repolarizing currents depicted. Terfenadine inhibits IKr current, thereby prolonging the ventricular action potential. (b) Atrial and ventricular m-mode recorded from control and MO19b-injected Tg(Myl7:GFP) zebrafish embryos after 30 μM Terfenadine treatment. (b,c) 25% ± 4.1% of miR-19b deficient embryos develop an AV-Block with the ventricle skipping every other contraction, whereas control injected embryos show no phenotype. (±sd; n = 3 with ≥10 animals per group; p < 0.05) (d,e) Patch-clamp Experiments revealed that morpholino-mediated loss of miR-19b results in prolonged action potentials with up to 57% ± 3.8% and 39% ± 3.5% prolongation of APD50 and APD90, respectively (±sd; n ≥ 10 from 5 hearts; p < 0.05). Additionally, the notch appeared to be less pronounced (stars).