Modification of sodium channel inactivation in single myelinated nerve fibers by methionine-reactive chemicals.
Several methionine-reactive reagents, including N-bromoacetamide, N-bromosuccinimide, chloramine-T, and N-chlorosuccinimide, irreversibly slowed and prevented Na channel inactivation in single myelinated nerve fibers, whereas sulfhydryl- or tyrosine-modifying reagents had little effect. The activation process was not modified by the reagents that altered inactivation and could be modulated normally by Ca++ ions and Centruroides scorpion toxin II alpha. These results suggest that externally applied N-bromoacetamide and its related compounds specifically affect Na channel inactivation by modifying methionine residues of the channel.
D000081:Acetamides / Q000494:pharmacology; D000818:Animals; D001974:Bromosuccinimide / Q000494:pharmacology; D002024:Bufo marinus; D002700:Chloramines / Q000494:pharmacology; D049832:Decapodiformes; D004228:Dithionitrobenzoic Acid / Q000494:pharmacology; D005033:Ethylmaleimide / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D008715:Methionine / Q000378:metabolism*; D009413:Nerve Fibers, Myelinated / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D013388:Succinimides / Q000494:pharmacology; D014105:Tosyl Compounds
D000081:Acetamides; D002700:Chloramines; D007473:Ion Channels; D013388:Succinimides; D014105:Tosyl Compounds; C016300:chloramine-T; C016272:N-bromoacetamide; C015752:N-chlorosuccinimide; D004228:Dithionitrobenzoic Acid; D012964:Sodium; D008715:Methionine; D001974:Bromosuccinimide; D005033:Ethylmaleimide