Abstract
Recent studies suggest that the neuronal nicotinic acetylcholine receptors present on chromaffin cells contain a 1,4-dihydropyridine-sensitive site whose occupation blocks membrane depolarization (1). In the present study, several L-type Ca2+ channel blockers inhibited the activation of the nAChRs present in the human neuroblastoma cell line, IMR 32, in a dose-dependent manner with IC50 values ranging from 0.8-3 microM. In contrast, omega-Conotoxin GVIA and omega-Agatoxin IVA had no effect up to 100 microM. Furthermore, the inorganic channel blocker, cadmium, had no effect either alone or on the modulatory role of the L-type antagonists, suggesting that the effects of these agents on nAChRs are not mediated via an interaction with calcium channels but possibly via a direct interaction with the nAChR ionophore.
MeSH terms
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
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Cadmium / pharmacology
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Calcium Channel Blockers / pharmacology*
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Calcium Channels / physiology*
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Diltiazem / pharmacology
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Humans
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Isradipine / pharmacology
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Neuroblastoma
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Neurons / physiology*
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Nicotine / pharmacology
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Nifedipine / pharmacology
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Nimodipine / pharmacology
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Peptides / pharmacology
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Receptors, Nicotinic / drug effects*
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Receptors, Nicotinic / physiology*
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Spider Venoms / pharmacology
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Tumor Cells, Cultured
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Verapamil / pharmacology
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omega-Agatoxin IVA
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omega-Conotoxin GVIA
Substances
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Calcium Channel Blockers
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Calcium Channels
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Peptides
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Receptors, Nicotinic
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Spider Venoms
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omega-Agatoxin IVA
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Cadmium
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Nimodipine
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Nicotine
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
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omega-Conotoxin GVIA
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Verapamil
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Diltiazem
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Nifedipine
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Isradipine