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In our previous studies, the evoked purine outflow from rat brain cultured astrocytes was reported to be Na+ independent and K+ and [Ca2+]e partially dependent. Thus, the eventual [Ca2+]i influence on purine astrocyte release was investigated in an attempt to better characterize the ionic requirements of this mechanism in cells which serve many complex and still partly unknown functions within the CNS. TMB-8 and Thapsigargin (drugs described as able to inhibit and increase the ion efflux from its internal stores respectively) and BAPTA/AM (able to chelate the cytoplasmic free Ca2+), were used. TMB-8 and BAPTA/AM decreased, whereas Thapsigargin enhanced glial purine outflow. These findings suggest a significant [Ca2+]i dependence of the electrically evoked purine efflux from cultured astrocytes even though further investigations using fluorescent probes are needed.
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