Sodium channel inactivation in squid axon is removed by high internal pH or tyrosine-specific reagents.
In squid axon, internal alkalinization from pH 7.1 to pH 10.2 results in a reversible decrease of the maximum inward current and the steady state sodium channel inactivation. Similar effects were observed after treatment of the axon with tetranitromethane or after iodination with lactoperoxidase. These results suggest that a tyrosine residue is an essential component of the inactivation process in this nerve.
D000818:Animals; D001369:Axons / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D049832:Decapodiformes; D004553:Electric Conductivity; D006860:Hydrogen Bonding; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007454:Iodides / Q000378:metabolism; D007784:Lactoperoxidase / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D013774:Tetranitromethane / Q000494:pharmacology; D014443:Tyrosine / Q000037:antagonists & inhibitors*
D007454:Iodides; D014443:Tyrosine; D012964:Sodium; D007784:Lactoperoxidase; D013774:Tetranitromethane