Cardiac excitation is dynamically controlled by the autonomic nervous system, i.e., sympathetic and parasympathetic nerves, through G-protein coupled receptor-dependent modulation of membrane ion channels. The signaling mechanisms are composed of cardiac GPCRs (β-adrenergic and m2-muscarinic receptors), G proteins (Gs and PTX-sensitive GK), intracellular cell-signaling molecules and the target ion channels (L-type Ca²⁺ channel and G protein-gated K⁺ channel). For quantitative understanding of the neural control of cardiac excitation, we developed mathematical models for parasympathetic deceleration of heart beat. Muscarinic activation of KG channels has been modeled based on our own experimental data. KG channels are activated directly by the βγ subunits of GK coupled to m2 receptors. The model is composed of two parts: one is for the interaction between G_βγ and KG channel, and the other is for m2 receptor and G proteins. Our recent finding on the role of RGS proteins in the control of GK activity has allowed us to construct the models reasonably reproducing temporal behavior of ACh-activation of KG channels. This model may be useful for quantitative understanding of neural control of cardiac excitation. [J Physiol Sci. 2008;58 Suppl:S177]