Calcium currents in a fast-twitch skeletal muscle of the rat.

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Abstract
Slow ionic currents were measured in the rt omohyoid muscle with the 3-microelectrode voltage-clamp technique. Na and delayed rectifier K currents were blocked pharmacologically. Under these conditions, depolarizing test pulses elicited an early outward current, followed by a transient slow inward current, followed in turn by a late outward current. The early outward current appeared to be a residual delayed rectifier current. The slow inward current was identified as a Ca current on the basis that its magnitude depended on extracellular Ca concentration, it was blocked by the addition of the divalent cations Cd or Ni, and reduced in magnitude by the addition of Mg or Co, and (c) Ba was able to replace Ca as an inward current carrier. The threshold potential for inward Ca current was around -20 mV in 10 mM extracellular Ca and .apprx. -35 mV in 2 mM Ca. Currents were net inward over part of their time course for potentials up to at least +30 mV. At temperatures of 20-26.degree. C, the peak inward current (at .apprx. 0 mV) was 139 .+-. 14 .mu.A/cm2 (mean .+-. SD), increasing to 226 .+-. 28 .mu.A/cm2 at temperatures of 27.degree.-37.degree. C. The late outward current exhibited considerable fiber-to-fiber variability. In some fibers, it was primarily a time-independent, nonlinear leakage current. In other fibers it appeared to be the sum of both leak and a slowly activated outward current. The rate of activation of inward Ca current was strongly temperature dependent. For example, in a representative fiber, the time-to-peak inward current for a +10-mV test pulse decreased from .apprx. 250 ms at 20.degree. C to 100 ms at 30.degree. C. At 37.degree. C, the time-to-peak current was typically .apprx. 25 ms. The earliest phase of activation was difficult to quantify because the ionic current was partially obscured by nonlinear charge movement. At physiological temperatures, the rate of Ca channel activation in rat skeletal muscle is .apprx. 5 times faster than activation of Ca channels in frog muscle. This pathway may be an important source of Ca entry in mammalian muscle.