Immobilization of membrane charge in frog skeletal muscle by prolonged depolarization.

Abstract

Inactivation (immobilization) of the non-linear component of capacitive current in semitendinosus muscles of R. pipiens was studied using the 3-micro-electrode voltage-clamp technique (Adrian, et al, 1970). The steady-state voltage dependence of non-linear charge immobilization was determined by changing the holding potential. The data were fitted to an equation analogous to that used to describe the charge activation process (Schneider et Chandler, 1973). The steepness parameter, k, is the same for charge activation and immobilization, but the mid-point voltage of charge immobilization is 8.9 .+-. 2.6 mV (n = 9) more negative than the mid-point of the non-linear charge activation curve. The charge relaxation rate constants are unaffected by changes in holding potential. The time course of non-linear charge immobilization was studied using a protocol that measures the change in capacitive current required for a voltage step of a fixed magnitude determined before and after an intervening period of depolarization. The sum of the non-linear charge that is immobilized and the non-linear charge that remains mobile after a prolonged (> 1 s) depolarization is equal to the total non-linear charge measured at a normally polarized holding potential (-80 mV). The determination of the quantity of charge immobilized does not require the assumption of linearity of the control capacity transient. The exponential time constant of charge immobilization was steeply voltage dependent. The charge immobilization time constant was 4.4 s at -40 mV 1.5 s at -20 mV and 0.28 s at +20 mV. Temperature was 5.degree. C. In addition to a decrease in the magnitude of non-linear capacitive charge during prolonged depolarization muscle fibers generally showed an apparent decrease in linear effective capacity. This apparent change and the increase previously reported to occur when chronically depolarized fibers are hyperpolarized (Rakowski, 1978) may be artifactual results of incorrect current scaling rather than changes that result from alteration of a conductance pathway from the transverse tubular system into the sarcoplasmic reticulum.