Gallamine triethiodide‐induced modifications of sodium conductance in Myxicola giant axons.

Publisher Website
Google Scholar
Abstract
Internal gallamine triethiodide (Flaxedil) modified Na+ channel kinetics in Myxicola axons but does not alter the K+ conductance. The drug has no effect externally. Gallamine initially increases the leakage conductance, but this effect completely reverses within 30 min despite the maintained presence of drug. During step depolarizations to membrane potentials < -10 mV, gallamine slows the rate of Na+ inactivation, but all channels which have opened can still inactivate. During depolarizations to more positive potentials, gallamine-modified Na+ currents show a biphasic decline, and at Vmax > -10 mV. Na+ inactivation is incomplete as evidenced by the large Na+ tail currents which follow pulses sufficiently long to have allowed complete inactivation of normal Na+ channels. The tail currents are slower than normal Na+ tails, and exhibit a pronounced hook. With gallamine, the fraction of Na+ channels which do not inactivate increases sigmoidally over the range 0-80 mV. For Vmax > ENa, gallamine almost completely blocks outward Na+ currents. The block is determined by the direction of Na+ current, rather than the absolute membrane potential. Gallamine has no effect upon the rate of Na+ channel activation, the maximum Na+ conductance, the steady-state Na+ inactivation curve, or the rate of development or removal of inactivation by prepulses. Gallamine eliminates physiological immobilization of intramembrane charge movements (QOFF and QON) and does not itself induce immobilization. In the presence of gallamine, QOFF following long pulses is the same as QOFF following short pulses.