Nature 364, 802 - 806 (26 August 1993); doi:10.1038/364802a0

Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel

Yoshihiro Kubo^*, Eitan Reuveny, Paul A. Slesinger, Yuh Nung Jan & Lily Y. Jan

Howard Hughes Medical Institute and Departments of Physiology and Biochemistry, University of California, San Francisco, California 94143-0724, USA
^*Present address: Department of Neurophysiology, Tokyo Metropolitan Institute for Neuro-science, Musashidai 2-6, Fuchu-ciry, Tokyo 183, Japan.

PARASYMPATHETIC nerve stimulation causes slowing of the heart rate by activation of muscarinic receptors and the subsequent opening of muscarinic K⁺ channels in the sinoatrial node and atrium^1–4. This inwardly rectifying K⁺ channel is coupled directly with G protein^5–10. Based on sequence homology with cloned inwardly rectifying K⁺ channels, ROMK1 (ref. 11) and IRK1 (ref. 12), we have isolated a complementary DNA for a G-protein-coupled inwardly rectifying K⁺ channel (GIRK1) from rat heart. The GIRK1 channel probably corresponds to the muscarinic K channel because (1) its functional properties resemble those of the a trial muscarinic K⁺ channel and (2) its messenger RNA is much more abundant in the atrium than in the ventricle. In addition, GIRK1 mRNA is expressed not only in the heart but also in the brain.

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