Abstract

Charge movement and calcium transient were measured simultaneously in stretched frog cut twitch fibers under voltage clamp, with the internal solution containing 20mM EGTA plus added calcium and antipyrylazo III. When the nominal free [Ca2+]i was 10nM, the shape of the broad Iγ hump in the ON segments of charge movement traces remained invariant when the calcium release rate was greatly diminished. When the nominal free [Ca2+]i was 50nM, which was close to the physiological level, the Iγ humps were accelerated and a slow calcium-dependent Iδ component (or state) was generated. The peak of ON Iδ synchronized perfectly with the peak of the calcium release rate whereas the slow decay of ON Iδ followed the same time course as the decay of calcium release rate. Suppression of calcium release by TMB-8 reduced the amount of Qδ concomitantly but not completely, and the effects were partially reversible. The same simultaneous suppression effects were achieved by depleting the sarcoplasmic reticulum calcium store with repetitive stimulation. The results suggest that the mobility of Qδ needs to be primed by a physiological level of resting myoplasmic Ca2+. Once the priming is completed, more Iδ is mobilized by the released Ca2+ during depolarization.

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