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.
Joshi
P G
PG
Department of Biophysics, National Institute of Mental Health and Neurosciences, Bangalore, India.
Mishra
S
S
D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000737:chemistry*; D002413:Cations, Divalent; D005699:Galactosylceramides / Q000502:physiology*; D005910:Glioma; D006801:Humans; D007158:Immunologic Techniques; D015640:Ion Channel Gating; D008345:Manganese / Q000378:metabolism; D019284:Thapsigargin / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002413:Cations, Divalent; D005699:Galactosylceramides; D008345:Manganese; D019284:Thapsigargin; D014700:Verapamil; D002118:Calcium