A Toxin Fraction (FTX) from the Funnel-Web Spider Poison Inhibits Dihydropyridine-Insensitive Ca2+ Channels Coupled to Catecholamine Release in Bovine Adrenal Chromaffin Cells

• Autor(a) principal: Duarte, Carlos B.
• Data de Publicação: 1993
• Outros Autores: Rosário, Luís M., Sena, Cristina M., Carvalho, Arsélio P.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/8331; https://doi.org/10.1111/j.1471-4159.1993.tb03236.x

In adrenal chromaffin cells, depolarization-evoked Ca2+ influx and catecholamine release are partially blocked by blockers of L-type voltage-sensitive Ca2+ channels. We have now evaluated the sensitivity of the dihydropyridine-resistant components of Ca2+ influx and catecholamine release to a toxin fraction (FTX) from the funnel-web spider poison, which is known to block P-type channels in mammalian neurons. FTX (1:4,000 dilution, with respect to the original fraction) inhibited K+-depolarization-induced Ca2+ influx by 50%, as monitored with fura-2, whereas nitrendipine (0.120131 03BCM) and FTX (3:3), a synthetic FTX analogue (1 mM), blocked the [Ca2+]i transients by 35 and 30%, respectively. When tested together, FTX and nitrendipine reduced the [Ca2+]i transients by 70%. FTX or nitrendipine reduced adrenaline and noradrenaline release by 223C80 and 70%, respectively, but both substances together abolished the K+-evoked catecholamine release, as measured by HPLC. The 03C9-conotoxin GVIA (0.5 03BCM) was without effect on K+-stimulated 45Ca2+ uptake. Our results indicate that FTX blocks dihydropyridine- and 03C9-conotoxin-insensitive Ca2+ channels that, together with L-type voltage-sensitive Ca2+ channels, are coupled to catecholamine release.