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Here we used cultured C6 glioma cells to investigate the possibility that 5\u2010HT<jats:sub>2A<\/jats:sub> receptors on glia regulate glutamate release from the cell. The efflux of endogenous glutamate from cultured C6 glioma cells was increased by addition of 5\u2010HT in a concentration\u2010dependent manner (maximal effect +200%). The efflux of serine and aspartate was not altered. The effect of 5\u2010HT was mimicked by both the nonselective 5\u2010HT receptor agonist quipazine and the selective 5\u2010HT<jats:sub>2<\/jats:sub> receptor agonist 4\u2010iodo\u20102,5\u2010dimethoxyamphetamine (DOI; both 0.01\u2013100 \u03bcM). The 5\u2010HT<jats:sub>2A<\/jats:sub> receptor antagonists ketanserin (1 \u03bcM) and spiperone (1 \u03bcM) inhibited the glutamate response to 5\u2010HT, quipazine, and DOI, whereas the effect of 5\u2010HT was not inhibited by the 5\u2010HT<jats:sub>2B\/C<\/jats:sub> receptor antagonist SB200646 (1 \u03bcM). The effect of 5\u2010HT on glutamate was specific in that it was reduced in low\u2010calcium medium but was not prevented by furosemide (5 mM), which prevents cell swelling\u2010induced glutamate release. Finally, the glutamate uptake inhibitor 2,4,trans\u2010pyrollidine dicarboxylic acid (50 \u03bcM) did not block the 5\u2010HT\u2010induced efflux of glutamate, making involvement of glutamate transport unlikely. In conclusion, 5\u2010HT stimulates the efflux of glutamate from C6 glioma cells following 5\u2010HT<jats:sub>2A<\/jats:sub> receptor activation and involves a calcium\u2010dependent mechanism. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.10126","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T23:45:33Z","timestamp":1030319133000},"page":"399-405","source":"Crossref","is-referenced-by-count":38,"title":["In vitro evidence that 5\u2010hydroxytryptamine increases efflux of glial glutamate via 5\u2010HT<sub>2A<\/sub> receptor 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