Fig 3.
Ultralong action potentials in guinea pig myocytes lacking CDI. (A) Exemplar action potentials (APs) in uninfected cells (NV), and in cells with AdIR-CaMs (WT, CaMWT+GFP; 12, CaM12+GFP; 34, CaM34+GFP; 1234, CaM1234+GFP). Gray line, voltage for APD (APD) measurement. Waveform differences for WT, 12, and NV illustrate variability observable within any one of groups; group means are statistically indistinguishable in B. Likewise, 34 and 1234 exemplars illustrate variability present in either group; there is no statistical difference of groups means in B. (B) Mean APDs, from populations relating to exemplars in A. APDs for NV, WT, and 12 were statistically indistinguishable, as were those for 34 and 1234. APD differences between these two groups were significant. (C) Engineered CaMs eliminate CDI in guinea pig cells. Exemplar L-type currents from uninfected cells (Left), and those with AdIR-CaM1234 (Right); format is as in Fig. 1C Top. Mean f below indicates approximately complete elimination of CDI by CaM1234. (D) No K current change by engineered CaMs in guinea pig cells. (Left), Uninfected cells. (Right) Cells with AdIR-CaM1234. (Upper) Exemplar K currents during steps to marked voltages, from −70 mV holding potential. (Lower) K current-voltage curves, averaged from n cells in each population. •, Peak K currents at voltage-pulse onset; ○, K currents at end of 2-s pulses. (E) No APD prolongation by CaM1234 with nimodipine (10 μM). Bar graph, format as in B; APDs with nimodipine are significantly shorter than counterparts in B; there is no statistical difference between NV and 1234 in E. (Left Inset) AP in NV exemplar cell, ±nimodipine (±DHP). (Right Inset), exemplar NV and 1234 (gray) APs with nimodipine.