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- Title
Calcium-independent phospholipase A<sub>2</sub> mediates store-operated calcium entry in rat cerebellar granule cells.
- Authors
Singaravelu, Karthika; Lohr, Christian; Deitmer, Joachim W.
- Abstract
Store-operated Ca2+ entry (SOCE) has been extensively studied in non-neuronal cells, such as glial cells and smooth muscle cells, in which Ca2+-independent phospholipase A2 (iPLA2) has been shown to play a key role in the regulation of SOCE channels. In the present study, we have investigated the role of iPLA2 for store-operated Ca2+ entry in rat cerebellar granule neurons in acute brain slices using confocal Ca2+ imaging. Depletion of Ca2+ stores by cyclopiazonic acid (CPA) induced a Ca2+ influx, which could be inhibited by SOCE channel blockers 2-aminoethoxy-diphenylborate (2-APB) and 3,5-bistrifluoromethyl pyrazole derivative (BTP2), but not by the voltage-operated Ca2+ channel blocker diltiazem and by the Na+ channel blocker tetrodotoxin. The inhibitors of iPLA2, bromoenol lactone (BEL) and 1,1,1-trifluoro-2-heptadecanone, and the selective suppression of iPLA2 expression by antisense oligodeoxynucleotides, inhibited CPA-induced Ca2+ influx. Calmidazolium, which relieves the block of inhibitory calmodulin from iPLA2, elicited a Ca2+ influx similar to CPA-induced Ca2+ entry. The product of iPLA2, lysophosphatidylinositol, elicited a 2-APB- and BTP2-sensitive, but BEL-insensitive, Ca2+ influx. Spontaneous Ca2+ oscillations in granule cells in acute brain slices were reduced after inhibiting iPLA2 activity or by blocking SOCE channels. The results suggest that depletion of Ca2+ stores activates iPLA2 to trigger Ca2+ influx by the formation of lysophospholipids in these neurons.
- Subjects
CELLS; BRAIN; NEURONS; NEURAL circuitry; NEURAL stem cells
- Publication
Cerebellum, 2008, Vol 7, Issue 3, p467
- ISSN
1473-4222
- Publication type
Article
- DOI
10.1007/s12311-008-0050-z