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Extracellular ATP Stimulates Calcium Influx in Neuroblastoma Glioma Hybrid NG108–15 Cells

Abstract— ATP‐induced changes in the intracellular Ca2+concentration ([Ca2+]i) in neuroblastoma glioma hybrid NG108–15 cells were studied. Using the fluorescent Ca2+indicator fura‐2, we have shown that the [Ca2+]i increased in response to ATP. ATP at 3 mM caused the greatest increase in [Caz+]i, whereas at higher concentrations of ATP the response became smaller. Two nonhydrolyzable ATP analogues, adenosine 5′‐thiotriphosphate and 5′‐adenylyl‐β, γ‐imidodiphosphate, could not trigger significant [Ca2+]i change, but they could block the ATP effect. Other adenine nucleotides, including ADP, AMP, α,β‐methylene‐ATP, β,γ‐methylene‐ATP, and 2‐methylthio‐ATP, as well as UTP and adenosine, all had no effect on [Ca2+]i at 3 mM. In the absence of extracellular Ca2+, the effect of ATP was inhibited totally, but could be restored by the addition of Ca2+ to the cells. Upon removal of Mg2+, the maximum increase in [Ca2+]i induced by ATP was enhanced by about 42%. Ca2+‐channel blockers partially inhibited the ATP‐induced [Ca2+]i rise. The ATP‐induced [Ca2+]i rise was not affected by thapsigargin pretreatment, though such pretreatment blocked bradykinin‐induced [Ca2+]i rise completely. No heterologous desensitization of [Ca2+]i rise was observed between ATP and bradykinin. The magnitude of the [Ca2+]i rise induced by ATP increased between 1.5 and 3.1 times when external Na+was replaced with Tris, N‐methyl‐d‐glucamine, choline, or Li+. The addition of EGTA or verapamil to cells after their maximum response to ATP immediately lowered the [Ca2+]i to the basal level in Na+‐containing or Na+‐free Tris solution. Our results suggest that ATP stimulates Ca2+influx via at least two pathways: ion channels that are permeable to Ca2+ and Na+, and pores formed by ATP4‐.