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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Selective antagonism of human 5-HT1D and 5-HT1B receptor-mediated responses in stably transfected C6-glial cells by ketanserin and GR 127,935.

The antagonist effects of ketanserin and 2'-methyl-4'-(5-methyl-1,2,4)oxadiazol-3-yl)-biphenyl-[4-carboxyli c acid 4-methoxy-3-(4-methyl-piperazin-1-yl)-phenyl]-amide (GR 127,935) were compared to naratriptan-induced inhibition of cAMP formation in C6-glial cell lines stably expressing human 5-HT1D or 5-HT1B receptor sites. Ketanserin demonstrated potent (pA2: 7.76), competitive antagonism of naratriptan-induced inhibition of forskolin (100 microM)-stimulated cAMP formation in C6-glial/5-HT1D cells. Whereas GR 127,935 was ineffective as an antagonist in these cells, it produced and intrinsic activity (pEC50: 6.98) that was sensitive to ketanserin (10 microM) blockade. Unlike ketanserin, GR 127,935 potently antagonised the naratriptan response in C6-glial/5-HT1B cells while also depressing the maximum response. The differential antagonist effects of ketanserin and GR 127,935 on naratriptan responses elicited in C6-glial/5-HT1D and C6-glial/5-HT1B cells demonstrate these compounds do selectively block human 5-HT1D and 5-HT1B receptors, respectively.[1]


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