Sodium-channels in Non-excitable Glioma Cells, Shown by the Influence of Veratridine, Scorpion Toxin, and Tetrodotoxin on Membrane Potential and on Ion Transport

Overview

Journal Pflugers Arch

Specialty Physiology

Date 1983 Jun 1

PMID 6310481

Citations 8

Authors

G Reiser

B Hamprecht

Affiliations

Soon will be listed here.

Abstract

Veratridine induces membrane potential oscillations in non-excitable glioma cells, which are not affected by ouabain (2 mM) or by D600 (0.1 mM). In the presence of veratridine, scorpion toxin causes depolarization of the glioma cells to a positive value of the membrane potential. These effects of veratridine and of scorpion toxin are observed in Na+ but not in choline medium and are inhibited by tetrodotoxin. The response of the glioma cells to bradykinin has also been studied during these experiments. Previously bradykinin has been shown in these cells to induce a hyperpolarizing response caused by an increase in K+ conductance. This response to bradykinin can still be seen during the veratridine-induced oscillations of the membrane potential. In the glioma cells the uptake of guanidinium, a substitute for Na+, is enhanced by veratridine plus scorpion toxin. This stimulation is tetrodotoxin-sensitive. However, in the excitable neuroblastoma X glioma hybrid cells studied for comparison, veratridine causes membrane potential oscillations accompanied at the rising phase by one action potential or a train of action potentials. The results demonstrate that in non-excitable glioma cells tetrodotoxin-sensitive Na+ channels can be activated by veratridine and by scorpion toxin.

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