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Journal of Neuroscience, Vol 7, 1613-1625, Copyright © 1987 by Society for Neuroscience
Nerve growth factor increases the number of functional Na channels and induces TTX-resistant Na channels in PC12 pheochromocytoma cells
B Rudy, B Kirschenbaum, A Rukenstein and LA Greene
The PC12 clone is a line of rat pheochromocytoma cells that undergoes
neuronal differentiation in the presence of NGF protein. In the absence of
NGF, PC12 cells are electrically inexcitable, while after several weeks of
NGF treatment they develope Na+ action potentials. Past estimates made by
measuring binding of 3H-saxitoxin (STX) indicate that NGF treatment brings
about a large increase in Na channel density that is of sufficient
magnitude to account for the induction of excitability. We have now used
22Na uptake to measure the Na permeability of PC12 cells before and after
long-term NGF treatment. Treatment with NGF does not change the resting Na+
permeability. The alkaloid toxins veratridine and batrachotoxin (BTX) and
scorpion toxin were used to activate Na channels. Such studies demonstrate
that these toxins induce TTX-sensitive Na uptake in both NGF-treated and
untreated cells and reveal differences in functional Na channel numbers per
cell and per unit of membrane area that are similar to those found in the
STX binding studies. On the other hand, affinities for drugs that activate
these channels are not affected by NGF treatment. We also find that
NGF-treated PC12 cells contain a population of Na channels with low
affinity for TTX. These channels account for 5-20% of total BTX or
veratridine-stimulated flux. Thus, NGF has 2 effects regarding the Na
channels of PC12 cells: it increases the number of functional Na channels
that otherwise behave similarly to those present before NGF treatment, and
it induces the presence of TTX-resistant Na channels. These findings
indicate that the PC12 model system may serve to study the developmental
regulation of Na channel expression and properties.
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