title: Calcium mobilization and entry by thapsigargin in neuronal tumor cell line, SK-N-SH.
abstract: Using fura-2 loaded neural tumour cells, SK-N-SH, we demonstrate that receptor-mediated activation of phosphoinositide hydrolysis not only causes the release of Ca2+ from intracellular stores but also causes a concomitant influx of extracellular Ca2+. Thapsigargin (TG), a sesquiterpene lactone, causes a sustained elevation of intracellular Ca2+ and depletion of the inositol 1, 4, 5-trisphosphate-sensitive intracellular Ca2+ stores. In the absence of extracellular Ca2+, the increase in intracellular Ca2+ concentration ([Ca2+]i) was transient, suggesting that thapsigargin activates both intracellular mobilization and the influx of Ca2+ from extracellular space. These results are consistent with the proposal that the depletion of the inositol 1, 4, 5-trisphosphate-sensitive intracellular Ca2+ pool serves as a signal for Ca2+ influx.
authors.affiliation: Department of Pharmacology, ICI Pharmaceuticals Group, ICI Americans Inc., Wilmington, Delaware.
authors.forename: W C
authors.initials: WC
authors.lastname: Moore
authors.forename: H M
authors.initials: HM
authors.lastname: Hargrove
authors.forename: A I
authors.initials: AI
authors.lastname: Salama
authors.forename: J
authors.initials: J
authors.lastname: Patel
mesh_terms: D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002217:Carbachol / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D007295:Inositol Phosphates / Q000096:biosynthesis; D009474:Neurons / Q000378:metabolism*; D013729:Terpenes / Q000494:pharmacology*; D019284:Thapsigargin; D014407:Tumor Cells, Cultured
chemical_list: D007295:Inositol Phosphates; D013729:Terpenes; D004533:Egtazic Acid; D019284:Thapsigargin; D002217:Carbachol; D000252:Calcium-Transporting ATPases; D002118:Calcium