A novel type of Ca2+ channel in U-87 MG cells activated by anti-galactocerebroside

Antibody to galactocerebroside (GalC) evokes a Ca2+ response in cultured glioma U-87 MG cells. The rise in intracellular calcium [Ca2+]i occurs largely due to the influx of Ca2+ through a plasma membrane channel, though the release of Ca2+ from intracellular stores also contributes. We characterized the channel activated by anti-GalC. The channel activity was transient and the inactivation appeared to be Ca2+ dependent. The channel was impermeant to monovalent ions Na+ and K+ and also to Mn2+. Ni2+ and Co2+ neither permeate through the channel nor inhibit the Ca2+ influx. In contrast Cd2+ the most potent inorganic blocker of Ca2+ channels permeated through this channel. The Ca2+ influx was inhibited by verapamil with IC50 of 65 +/- 8 microM. The Ca2+ influx as well as the intracellular release were markedly inhibited by neomycin sulfate and phorbol dibutyrate, suggesting that the Ca2+ influx may be mediated by IP3 (1). Depletion of intracellular Ca2+ stores by thapsigargin was followed by Ca2+ influx. This represents the capacitative Ca2+ entry pathway and is distinct from the channel activated by anti -GalC.