Author's present address I. C. Wood: School of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, UK.
Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors
Article first published online: 13 AUG 2004
The Journal of Physiology
Volume 522, Issue 3, pages 349–355, February 2000
How to Cite
Selyanko, A. A., Hadley, J. K., Wood, I. C., Abogadie, F. C., Jentsch, T. J. and Brown, D. A. (2000), Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M1 muscarinic acetylcholine receptors. The Journal of Physiology, 522: 349–355. doi: 10.1111/j.1469-7793.2000.t01-2-00349.x
- Issue published online: 13 AUG 2004
- Article first published online: 13 AUG 2004
- (Received 22 October 1999; accepted after revision 6 December 1999)
KCNQ1-4 potassium channels were expressed in mammalian Chinese hamster ovary (CHO) cells stably transfected with M1 muscarinic acetylcholine receptors and currents were recorded using the whole-cell perforated patch technique and cell-attached patch recording.
Stimulation of M1 receptors by 10 μm oxotremorine-M (Oxo-M) strongly reduced (to 0–10%) currents produced by KCNQ1-4 subunits expressed individually and also those produced by KCNQ2+KCNQ3 and KCNQ1+KCNE1 heteromers, which are thought to generate neuronal M-currents (IK,M) and cardiac slow delayed rectifier currents (IK,s), respectively.
The activity of KCNQ2+KCNQ3, KCNQ2 and KCNQ3 channels recorded with cell-attached pipettes was strongly and reversibly reduced by Oxo-M applied to the extra-patch membrane.
It is concluded that M1 receptors couple to all known KCNQ subunits and that inhibition of KCNQ2+KCNQ3 channels, like that of native M-channels, requires a diffusible second messenger.