Abstract
The major component of whole-cell Ca2+ current in differentiated, neuron-like rat pheochromocytoma (PC12) cells and sympathetic neurons is carried by dihydropyridine-insensitive, high-threshold-activated N-type Ca2+ channels. We show that these channels have unitary properties distinct from those of previously described Ca2+ channels and contribute both slowly inactivating and large sustained components of whole-cell current. The N-type Ca2+ currents are modulated by GTP binding proteins. The snail toxin omega-conotoxin reveals two pharmacological components of N-type currents, one blocked irreversibly and one inhibited reversibly. Contrary to previous reports, neuronal L-type channels are insensitive to omega-conotoxin. N-type Ca2+ channels appear to be specific for neuronal cells, since their functional expression is greatly enhanced by nerve growth factor.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Acetylcholine / pharmacology
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Animals
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Calcium / metabolism*
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Calcium Channels / drug effects
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Calcium Channels / physiology*
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Dihydropyridines / pharmacology
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GTP-Binding Proteins / metabolism
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Guanosine 5'-O-(3-Thiotriphosphate)
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Guanosine Triphosphate / analogs & derivatives
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Guanosine Triphosphate / pharmacology
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Ion Channel Gating / drug effects*
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Mollusk Venoms / pharmacology
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Neurons / metabolism
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Pheochromocytoma / pathology
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Rats
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Thionucleotides / pharmacology
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Tumor Cells, Cultured / metabolism
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omega-Conotoxins*
Substances
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Calcium Channels
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Dihydropyridines
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Mollusk Venoms
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Thionucleotides
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omega-Conotoxins
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Conus magus toxin
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Guanosine 5'-O-(3-Thiotriphosphate)
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1,4-dihydropyridine
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Guanosine Triphosphate
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GTP-Binding Proteins
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Acetylcholine
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Calcium