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GIRK channels control spike frequency in atrial pacemaker cells and inhibitory potentials in neurons. By directly responding to G proteins, PIP 2  and Na + , GIRK is under the control of multiple signaling pathways. In this study, the mammalian GIRK2 channel has been purified and reconstituted in planar lipid membranes and effects of Gα, Gβγ, PIP 2  and Na +  analyzed. Gβγ and PIP 2  must be present simultaneously to activate GIRK2. Na +  is not essential but modulates the effect of Gβγ and PIP 2  over physiological concentrations. Gα i1 (GTPγS) has no effect, whereas Gα i1 (GDP) closes the channel through removal of Gβγ. In the presence of Gβγ, GIRK2 opens as a function of PIP 2  mole fraction with Hill coefficient 2.5 and an affinity that poises GIRK2 to respond to natural variations of PIP 2  concentration. The dual requirement for Gβγ and PIP 2  can help to explain why GIRK2 is activated by G i/o , but not G q  coupled GPCRs.

Quantitative analysis of mammalian GIRK2 channel regulation by G proteins, the signaling lipid PIP 2 and Na + in a reconstituted system