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  • Title: Methoxyverapamil reduction of nicotine-induced catecholamine release involves inhibition of nicotinic acetylcholine receptor currents.
    Author: Boehm S, Huck S.
    Journal: Eur J Neurosci; 1993 Oct 01; 5(10):1280-6. PubMed ID: 8275230.
    Abstract:
    The mechanism by which the putative Ca2+ channel blocker methoxyverapamil (D600) inhibits nicotine-induced catecholamine release was investigated in bovine adrenal chromaffin cells and in neurons from paravertebral sympathetic ganglia of chick embryos. We found D600 to prevent catecholamine release evoked by 30 s applications of nicotine with a significantly higher potency than the release induced either by 30 s K+ depolarizations or by electrical field stimulation of sympathetic neurons. Like the use-dependent action of D600 upon Ca2+ channels, the magnitude of inhibition of the K(+)-evoked secretion depended on the duration of stimulation (10 s to 5 min). Data on catecholamine release were supplemented by patch-clamp recordings. We found whole-cell currents in chromaffin cells evoked by (extrapolated) 0.5 s applications of nicotine to be significantly more sensitive to D600 than Ca2+ currents induced by a 0.5 s depolarization from -80 to 0 mV. In both instances, the potency of D600 depended on the duration of the (nicotinic and depolarizing) stimuli. Our data suggest that D600 inhibits nicotine-induced catecholamine release by reducing nicotinic acetylcholine receptor currents rather than voltage-gated Ca2+ currents. Hence, in chromaffin cells as well as in sympathetic neuronal preparations, D600 does not appear to be a suitable tool to investigate the part voltage-activated Ca2+ currents play in cellular events induced by nicotine.
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