Abstract
The acute and long-term effects of ethanol on voltage-dependent Ca channel function were studied in PC12, a clonal cell line of neural crest origin. Acute exposure to ethanol produced a concentration-dependent decrease in depolarization-evoked 45Ca2+ uptake, while prolonged (2-10 days) exposure led to a reciprocal increase in 45Ca2+ uptake and in the number of Ca-channel binding sites labeled by the dihydropyridine Ca-channel antagonist [3H]nitrendipine. Uptake was restored to control levels following withdrawal of ethanol from cultures. These findings indicate that cellular adaptation to ethanol may involve enhanced expression of dihydropyridine-sensitive, voltage-dependent Ca channels.
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Selected References
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