Calcium mobilization and entry by thapsigargin in neuronal tumor cell line, SK-N-SH

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, caus...

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Bibliographic Details
Published in:	Neuroreport Vol. 2; no. 3; p. 124
Main Authors:	Moore, W C, Hargrove, H M, Salama, A I, Patel, J
Format:	Journal Article
Language:	English
Published:	England 01-03-1991
Subjects:	Calcium - antagonists & inhibitors Calcium - metabolism Calcium-Transporting ATPases - antagonists & inhibitors Carbachol - pharmacology Egtazic Acid - pharmacology Extracellular Space - metabolism Inositol Phosphates - biosynthesis Neurons - metabolism Terpenes - pharmacology Thapsigargin Tumor Cells, Cultured
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Summary:	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.
ISSN:	0959-4965
DOI:	10.1097/00001756-199103000-00003