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We have studied the ion flux through the sodium channels of low passage number (less than 50 p.) and high passage number (greater than 150 p.) neuroblastoma x glioma hybrid cells using [14C] guanidinium and specific neurotoxins to induce channel opening and closing. The sodium channels of low passage number hybrid cells could be opened by veratridine alone, suggesting the presence of voltage dependent channels in agreement with electrophysiological studies reported in the literature. The sodium channels of the high passage number hybrid cells, however, needed the synergistic action of veratridine and scorpion toxin for activation suggesting that these channels are "silent". The [14C] guanidinium ion flux through the sodium channels of the high passage number hybrid cells was inhibited by significantly lower concentrations of the volatile anesthetics (halothane, isoflurane and enflurane) and the local anesthetics (tetracaine and bupivacaine) than the comparable flux through the sodium channels of the low passage number hybrid cells.
P W Tas, and
H G Kress, and
K Koschel
July 1982,
FEBS letters,
P W Tas, and
H G Kress, and
K Koschel
July 1991,
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P W Tas, and
H G Kress, and
K Koschel
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P W Tas, and
H G Kress, and
K Koschel
April 1982,
FEBS letters,
P W Tas, and
H G Kress, and
K Koschel
January 1987,
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P W Tas, and
H G Kress, and
K Koschel
July 1997,
Neuroscience letters,
P W Tas, and
H G Kress, and
K Koschel
August 1981,
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P W Tas, and
H G Kress, and
K Koschel
January 1983,
Life sciences,
P W Tas, and
H G Kress, and
K Koschel
January 1989,
Progress in clinical and biological research,
P W Tas, and
H G Kress, and
K Koschel
April 1995,
Journal of neuroscience research,
