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Neurotoxins that cause persistent activation of voltage-sensitive sodium channels are highly cytotoxic to electrically excitable neuroblastoma cells. These toxins were used as selective agents to isolate variant neuroblastoma clones with missing or altered sodium channels. Of ten resistant clones analyzed, seven lacked functional sodium channels and one had a specific 40-fold increase Kd for scorpion toxin and altered voltage dependence of scorpion toxin binding. The phenotypes of these cell clones were stable for more than 100 generations, indicating that they were the result of stable genetic change.

Selection of variant neuroblastoma clones with missing or altered sodium channels.