Abstract
GH3cell lines stably expressing α1Echannel were established and the modulation of this channel by G-protein through membrane-delimited pathways was studied. α1Echannel expressed in GH3cells 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 GTPγS mimicked the action of these externally applied neurotransmitters, indicating that the α1Echannel 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 α1Achannel expressed in GH3cells. 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.
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More From: Biochemical and Biophysical Research Communications
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