Abstract
Voltage-sensitive sodium channels have a key role in the genesis of propagated action potentials. Mutations that affect these channels might be used like specific pharmacological agents in studies of channel structure and regulation. We have found that mutations which cause a reversible, temperature-induced paralysis in the fruit fly Drosophila melanogaster often affect the voltage-sensitive sodium channel. Using 3H-saxitoxin binding to membrane preparations, we have now identified two types of presumptive sodium channel mutants. One mutation, seizurets-2 (seits-2), appears to alter saxitoxin-binding sites structurally. The second, no-action-potential (napts) (refs 5, 6), reduces the number of saxitoxin-binding sites, but appears not to alter the receptor structure.
