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Inhibition of KCNQ1-4 potassium channels expressed in mammalian cells via M₁ muscarinic acetylcholine receptors

A. A. Selyanko, J. K. Hadley, I. C. Wood*, F. C. Abogadie*, T. J. Jentsch¹ and D. A. Brown

1. 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.

2. 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 (I_K,M) and cardiac slow delayed rectifier currents (I_K,s), respectively.

3. 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.

4. 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.