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T R Podleski

Publications and source records attributed to T R Podleski.

29 records · Page 2Linked to original sources
PubMed1976

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.

Action Potentials↗
PubMed1976

Lateral motion of fluorescently labeled acetylcholine receptors in membranes of developing muscle fibers.

We have made direct, quantitative measurements of the lateral motion and age-dependent distribution of acetylcholine receptors (AChR) on the surface of rat myotubes in primary culture. AChR were fluorescently marked with tetramethylrhodamine-labeled alpha-bungarotoxin and AChR lateral motion was measured by the fluoresence photobleaching recovery technique. We found two coexisting distinct classes of AChR: (i) mobile, uniformly distributed AChR that appear on all myotubes shortly after fusion from myoblasts; and (ii) immobile, dense, highly granular AChR in patches of 10-60 mum size that appear shortly after fusion and disappear after myotubes have become extensively interconnected. In addition, evidence of turnover of AChR labeled with tetramethylrhodamine-alpha-bungarotoxin is seen in the gradual internalization of surface fluorescence within 36 hr after labeling. The relevance of these results to an understanding of the membrane dynamics and localization of muscle AChR is discussed.

Age Factors↗
PubMed1976

Pharmacologic characterization of the Na+ ionophores in L6 myotubes.

We present a pharmacologic characterization of the Na+ ionophores present in L6 myotubes in vitro. Action potentials are abolished by replacement of the external Na+ by Tris. The amplitude of the action potential is generally resistant to high concentrations of tetrodotoxin (10(-5) M) and saxitoxin (10(-6 M), but the effect of these agents is highly variable. Veratridine (10(-4 M) consistently induces, as a short-term effect, a marked prolongation of the falling phase of the action potential. As a long-term effect, veratridine consistently induces a Na+-dependent reduction in the resting potential of the cell. The effects of veratridine on the action potential are not antagonized by tetrodotoxin or saxitoxin. However, the effects of veratridine on the resting potential are strongly antagonized by tetrodotoxin (10(-5) M) and fully inhibited by saxitoxin (10(-6) M). Significantly, under conditions where saxitoxin has fully inhibited the effects of veratridine on the resting potential, the myotubes are capable of generating overshooting action potentials. In contrast to their sensitivity to veratridine, L6 myotubes are insensitive to 10(-5) M alpha-dihydro-grayanotoxin-II. These results are discussed in the contexts of developmental significance and current views about Na+ ionophores.

Action Potentials↗