FIGURE 5.

Modulation of [Ca²⁺]_i oscillations in MIN6 cells by ATP and the P2Y antagonist MRS2179 unravels a possible mechanism of ATP action. (a) Addition of the P2Y antagonist MRS2179 (25 µM) to [Ca²⁺]_i oscillating MIN6 cells reduced and finally stopped [Ca²⁺]_i oscillations, indicating the essential role of ATP‐mediated P2Y stimulation for cell activity. (b) Treatment of MIN6 cells with MRS2179 (25 µM)––corresponding numbers of detected high‐intensity [Ca²⁺]_i events per 60 s interval. Shown are averages acquired from n = 50 MIN6 cells. (c) Addition of MRS2179 (50 µM) to mouse primary β‐cells reduced and stopped [Ca²⁺]_i oscillations. Findings on primary β‐cells compared well to observations on MIN6 cells. (d) Combined modulation of [Ca²⁺]_i oscillations by ATP and MRS2179. Addition of ATP (25 µM) to pre‐washed MIN6 cells‐stimulated [Ca²⁺]_i oscillations that were reduced and partly stopped by the P2Y antagonist MRS2179 (25 µM), probably by out‐competition of ATP from the receptor. Imaging was performed in the presence of 11 mM glucose for MIN6 cells and 5 mM glucose for mouse primary β‐cells