Detubulation effects on the action of zinc on frog skeletal muscle action potential

Detubulation of the untreated fiber decreases the time constant of the action potential's foot (τ _f ) and increases the maximal rate of rise of the spike ( $\dot V_{\max } $ ). Zinc at all concentrations, and regardless of whether the fiber is intact or detubulated, increases τ _f and decreases $\dot V_{\max } $ , and thus seems to decrease Na activation of the fiber. Detubulation was used principally to elucidate the localization and mechanism of the Zn²⁺-induced retardation of the falling phase of the frog sartorius fiber action potential, which evidently results from a general depression of delayed rectification. At 50 to 1000 μm, Zn²⁺ not only prolongs repolarization of intact fibers (measured by increase int _0.5, the half-time of the spike's fall), but also produces a marked hump early in this phase. Detubulation of zinc-free fibers reducest _0.5 to about 80% of its intact value, and under Zn²⁺ treatmentt _0.5 is increased but only to about 80% of that produced in the intact fiber, and the falling-phase hump is completely obliterated. Thus, detubulation decreasest _0.5 in Zn²⁺-treated fibers not only by generally eliminating T-tubular participation in action potential generation, but also by subtracting a Zn²⁺-induced retardation of tubular delayed rectification. Tubular delayed rectification must therefore be an intrinsic feature of normal excitation. These results are further analyzed by means of (i) Stanfield's findings about retardation of delayed rectification by Zn²⁺ and (ii) Adrian-Peachey's theory of T-tubule participation in action potential generation, which suggests that the Zn²⁺-evoked repolarization hump signals onset of Zn²⁺-altered active participation of T-tubules in determining the spike's shape.