These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Genetic and physiological evidence concerning the development of chemically sensitive voltage-dependent inophores in L6 cells.
    Author: Gartner TK, Land B, Podleski TR.
    Journal: J Neurobiol; 1976 Nov; 7(6):537-49. PubMed ID: 1003200.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]