Genetic and physiological evidence concerning the development of chemically sensitive voltage-dependent inophores in L6 cells.

The electrophysiological properties of a tissue culture muscle line, L6, and a K+ resistant mutant (MK1) derived from L6 were determined to elucidate certain aspects of membrane differentiation and function. MK1 was selected as a clone of myoblasts resistant to the toxic effects of 55 mM K+. The resting potentials of L6 and MK1 myoblasts and myotubes were K+ dependent and equal. The amplitudes of the action potentials were equal in normal medium, but 27.7 mM K+ interfered with or eliminated the ability of L6 myotubes to produce action potentials. MK1 myotubes produced nearly normal action potentials under these conditions. Thus, the K+ resistant myoblasts differentiate into myotubes which have an action potential generating mechanism much less sensitive to K+ than the normal mechanism. Also, both d-tubocurarine and alpha-bungarotoxin enhance the amplitude of the action potentials produced by L6 myotubes in the presence of 27.7 mM K+; these compounds do not enhance the amplitude of the action potentials produced by MK1 myotubes under the same conditions. It is proposed that as a consequence of differentiation a type of ionophore present in myoblasts becomes a voltage-dependent inophore in myotubes. Furthermore, these voltage-dependent ionophores can be chemically sensitive.