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.