Tunicamycin inhibits the expression of surface Na+ channels in cultured muscle cells.
We have investigated the effect of tunicamycin (TM), an inhibitor of protein glycosylation, on surface Na+ channels in cultured chick skeletal muscle cells. The expression of Na+ channels, estimated by the measurement of batrachotoxin (BTX)-activated 22Na+ uptake, was found to be significantly diminished after exposure of muscle cells to TM. This effect is partially reversed by the protease inhibitor leupeptin and is associated with a markedly enhanced rate of disappearance of Na+ channels from the surface of TM-treated cells. Our findings suggest that protein glycosylation contributes to the metabolic stability of voltage-sensitive Na+ channels.
D000818:Animals; D001496:Batrachotoxins / Q000494:pharmacology; D002478:Cells, Cultured; D002642:Chick Embryo; D003513:Cycloheximide / Q000494:pharmacology; D005944:Glucosamine / Q000031:analogs & derivatives*; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism; D009124:Muscle Proteins / Q000378:metabolism; D009132:Muscles / Q000378:metabolism*; D014415:Tunicamycin / Q000494:pharmacology*
D001496:Batrachotoxins; D007473:Ion Channels; D009124:Muscle Proteins; D014415:Tunicamycin; D003513:Cycloheximide; D005944:Glucosamine