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A Toxin Fraction (FTX) from the Funnel‐Web Spider Poison Inhibits Dihydropyridine‐Insensitive Ca 2+ Channels Coupled to Catecholamine Release in Bovine Adrenal Chromaffin Cells
Author(s) -
Duarte Carlos B.,
Rosario Luis M.,
Sena Cristina M.,
Carvalho Arsélio P.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03236.x
Subject(s) - nitrendipine , catecholamine , dihydropyridine , chemistry , chromaffin cell , depolarization , adrenal medulla , spider toxin , endocrinology , medicine , calcium , biophysics , biochemistry , biology , receptor , organic chemistry , glutamate receptor
In adrenal chromaffin cells, depolarization‐evoked Ca 2+ influx and catecholamine release are partially blocked by blockers of L‐type voltage‐sensitive Ca 2+ channels. We have now evaluated the sensitivity of the dihydropyridine‐resistant components of Ca 2+ 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 Ca 2+ influx by 50%, as monitored with fura‐2, whereas nitrendipine (0.1–1 μ M ) and FTX (3:3), a synthetic FTX analogue (1 m M ), blocked the [Ca 2+ ] i transients by 35 and 30%, respectively. When tested together, FTX and nitrendipine reduced the [Ca 2+ ] i transients by 70%. FTX or nitrendipine reduced adrenaline and noradrenaline release by ∼80 and 70%, respectively, but both substances together abolished the K + ‐evoked catecholamine release, as measured by HPLC. The ω‐conotoxin GVIA (0.5 μ M ) was without effect on K + ‐stimulated 45 Ca 2+ uptake. Our results indicate that FTX blocks dihydropyridine‐ and ω‐conotoxin‐insensitive Ca 2+ channels that, together with L‐type voltage‐sensitive Ca 2+ channels, are coupled to catecholamine release.