Depletion of Ca²⁺ stores by cyclopiazonic acid (CPA, 20 mM), induced store-operated Ca²⁺ entry (SOCE) in three cell types of rat cerebellum, Bergmann glia, astrocytes in granular cell layer and granule cells, has been studied in acute brain slices using confocal microscopy. The displacement of calmodulin (CaM) by the CaM antagonist calmidazolium (1 mM) also elicited Ca ²⁺ influx. The phospholipase A₂ inhibitor, bromoenol lactone (25 mM), and the SOCE channel blocker, 2-aminoethoxy-diphenylborate (100 mM) reduced or suppressed this Ca ²⁺ influx. The effect of different lysophospholipid products of iPLA₂ activity has been studied on Ca²⁺ influx. Lysophosphatidylcholine (LPC, 250 nM) and lysophosphatidylinositol (LPI, 250 nM) were more effective in inducing Ca²⁺ influx than lysophosphatidic acid (LPA, 250 nM). Our results suggest that iPLA₂ is a major regulator of SOCE in cerebellum; upon depletion of Ca²⁺ stores, iPLA₂ could be activated to open the channels in plasma membrane by the formation of lysophospholipids. Supported by the DFG (GPK 845/1 and SFB 530, B1)