Abstract
We recently reported that 5-hydroxytryptamine 2A (5-HT 2A) receptor activation on cultured glial cells induces glutamate release [J. Neurosci. Res. 67 (2002) 399]. Here we use C6 glioma cells to examine the role of calcium in this response. 5-Hydroxytryptamine (5-HT) increases glutamate release from C6 glioma cells, an effect blocked by low calcium conditions. The calcium ionophores ionomycin and calcimycin also released glutamate from C6 glioma cells in a Ca 2+-dependent manner. The effect of 5-HT was reduced by the phospholipase C inhibitor U73122 (1-[6[[(17β)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1 H-pyrrole-2,5-dione), but not its inactive enantomer U73343(1-[6[[(17β)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-2,5-pyrrolidinedione). The protein kinase C inhibitors staurosporine and calphostin C had no effect on the response to 5-HT, whereas the response was blocked by thapsigargin and caffeine. Neither the L-type calcium channel blockers, nifedipine and verapamil, nor the N-type calcium channel blocker ω-conotoxin GVIA inhibited the effect of 5-HT, whereas NiCl 2 and KCl blocked the response to 5-HT. We conclude that the 5-HT-induced efflux of glutamate from C6 glioma cells is Ca 2+-dependent and involves, at least in part, the mobilisation of Ca 2+ from inositol (1,4,5) tris phosphate (IP 3) sensitive intracellular stores.
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