Abstract
GH3 cell lines stably expressing alpha 1E channel were established and the modulation of this channel by G-protein through membrane-delimited pathways was studied. Alpha 1E channel expressed in GH3 cells showed slowing of activation and reduction of current amplitude by the application of carbachol or somatostatin. Both of these effects caused by these agents were pertussis toxin (PTX) sensitive and voltage dependent. Dialysis of the cell interior with GTP gamma S mimicked the action of these externally applied neurotransmitters, indicating that the alpha 1E channel is modulated by the PTX sensitive G-protein(s) through the membrane-delimited pathway but not by the PTX insensitive pathway that has been observed in alpha 1A channel expressed in GH3 cells. Thus different types of neuronal Ca2+ channels can be modulated not only by a similar mechanism but also by a different mechanism conferring a multilateral regulation of Ca2+ entry through these channels.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium Channel Blockers / pharmacology
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Calcium Channels / drug effects*
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Calcium Channels / genetics
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Calcium Channels / physiology
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Carbachol / pharmacology
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Cell Line
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Dihydropyridines / pharmacology
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Electric Conductivity
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GTP-Binding Proteins / physiology*
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Gene Expression
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Guanosine 5'-O-(3-Thiotriphosphate) / pharmacology
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Neurons / metabolism*
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Peptides / pharmacology
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Pertussis Toxin
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Pituitary Gland, Anterior / metabolism*
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Rats
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Somatostatin / pharmacology
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Spider Venoms / pharmacology
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Virulence Factors, Bordetella / pharmacology
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omega-Agatoxin IVA
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omega-Conotoxin GVIA
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omega-Conotoxins*
Substances
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Calcium Channel Blockers
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Calcium Channels
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Dihydropyridines
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Peptides
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Spider Venoms
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Virulence Factors, Bordetella
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omega-Agatoxin IVA
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omega-Conotoxins
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omega-conotoxin-MVIIC
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Guanosine 5'-O-(3-Thiotriphosphate)
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Somatostatin
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1,4-dihydropyridine
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Carbachol
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omega-Conotoxin GVIA
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Pertussis Toxin
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GTP-Binding Proteins