Studies on the role of calcium in the 5-HT-stimulated release of glutamate from C6 glioma cells.

Journal article

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[[(17 beta)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione), but not its inactive enantomer U73343(1-[6[[(17 beta)-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 omega-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.

Authors: Meller, R; Harrison, P; Sharp, T

• Publication status: Published
• Journal: European journal of pharmacology
• Volume: 445
• Issue: 1-2
• Pages: 13-19
• Publication date: 2002-06-01
• DOI: 10.1016/s0014-2999(02)01718-1
• EISSN: 1879-0712
• ISSN: 0014-2999
• Language: English
• Keywords: Tumor Cells, Cultured; Animals; Calcium; Calcium Channel Blockers; Serotonin; Glioma; Enzyme Inhibitors; Rats; Glutamic Acid