Abstract
The effects of actin cytoskeleton disruption by cytochalasin D and latrunculin A on Ca 2+ signals evoked by ADP, UTP or thapsigargin were investigated in glioma C6 cells. Despite the profound alterations of the actin cytoskeleton architecture and cell morphology, ADP and UTP still produced cytosolic calcium elevation in this cell line. However, calcium mobilization from internal stores and Ca 2+ influx through store-operated Ca 2+ channels induced by ADP and UTP were strongly reduced. Cytochalasin D and latrunculin A also diminished extracellular Ca 2+ influx in unstimulated glioma C6 cells previously incubated in Ca 2+ free buffer. In contrast, the disruption of the actin cytoskeleton had no effect on thapsigargin-induced Ca 2+ influx in this cell line. Both agonist- and thapsigargin-generated Ca 2+ entry was significantly decreased by the blocker of store-operated Ca 2+ channels, 2-aminoethoxydiphenylborate. The data reveal that two agonists and thapsigargin activate store-operated Ca 2+ channels but the mechanism of activation seems to be different. While the agonists evoke a store-mediated Ca 2+ entry that is dependent on the actin cytoskeleton, thapsigargin apparently activates an additional mechanism, which is independent of the disruption of the cytoskeleton.
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