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Blockade by Neurotransmitter Antagonists of Veratridine‐Activated Ion Channels in Neuronal Cell Lines
Author(s) -
Reiser Georg,
Günther Andrea,
Hamprecht Bernd
Publication year - 1983
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1983.tb11310.x
Subject(s) - veratridine , ionophore , chemistry , phentolamine , propranolol , neurotransmitter , biophysics , pharmacology , biochemistry , endocrinology , receptor , biology , sodium , sodium channel , organic chemistry , membrane
The voltage‐dependent Na + ionophore of various neuronal cells is permeable not only to Na + ions but also to guanidinium ions. Therefore, the veratridine‐(or aconitine‐) stimulated influx of [ 14 C]guanidinium in neuroblastoma × glioma hybrid cells was measured to characterize the Na + ionophore of these cells. Half‐maximal stimulation of guanidinium uptake was seen at 30 μ M veratridine. At 1 m M guanidinium, the veratridine‐stimulated uptake of guanidinium was lowered to 50% by approximately 60 m M Li + , Na + , or K + and by a few millimolar Mn 2+ , Co 2+ , or Ni 2+ . The basal, as well as the veratridine‐stimulated, uptake of guanidinium was inhibited by the cholinergic antagonists (+)‐tubocurarine ( K i = 50 to 500 n M ) and atropine ( K i = 5 to 30 μ M ) and the adrenergic antagonists phentolamine ( K i = 5 μ M ) and propranolol ( K i = 60 μ M ). The specificity of the inhibitory effects of these agents is stressed by the ineffectiveness of various other neurotransmitter antagonists. However, the corresponding ionophore in neuroblastoma cells (clone N1E‐115) seems to be regulated differently. While phentolamine and propranolol inhibit the veratridine‐activated uptake as in the hybrid cells, (+)‐tubocurarine and atropine exert only a slight effect.