Background: Transgenic mice have been increasingly utilized to investigate the molecular mechanisms of cardiac arrhythmias, yet the rate dependence and shape of the murine action potential restitution curve (ERC) remain undefined. Methods: Twenty-one isolated, Langendorff-perfused and AV-node ablated mouse hearts were studied. Left-ventricular and left-atrial action potentials were recorded using a validated miniaturized monophasic action potential (MAP) probe. Murine action potentials were measured at 30, 50, 70 and 90% repolarization (APD₃₀ to APD₉₀) during steady-state pacing and varied coupling intervals to determine ERCs. Results: Murine APD showed rate adaptation as well as restitution properties. The ERC time course differed dramatically between early and late repolarization: APD₃₀ shortened with increasing S1-S2 intervals, whereas APD₉₀ prolonged. When fitted by mono-exponential function, APD₃₀ reached plateau values significantly faster than APD₉₀ ( 29±2 vs. 78±6ms, p<0.01, n=12). The slope of early APD₉₀ restitution was significantly less than 1 (0.16±0.02). Atrial myocardium had shorter final repolarization, and significantly faster ERCs that were shifted leftward compared to ventricular myocardium. Recovery kinetics of intracellular Ca²⁺ transients recorded from isolated ventricular myocytes at 37 ° C ( 93±4ms, n=18) resembled the APD₉₀ ERC kinetics. Conclusions: Mouse myocardium shows AP cycle-length dependence and electrical restitution properties that are surprisingly similar to that of larger mammals and humans.