Cardiac gap junctions ensure the coordinated propagation of the action potential. They are clusters of intercellular channels (GJC) composed of connexins (Cxs) Cx40, Cx43, Cx45 and Cx30.2, which display specific electrical properties in the different tissues. In the diseased heart (e.g atrial and ventricular fibrillations), Cxs remodelling and altered pro-arrhythmic electrical properties have been observed.The aim of this study is to determine the role of each connexin in regulating the propagation of action potential. The mouse atrial phenotypic HL-1 cell line, owning a spontaneous contractile activity and that co-expresses Cx40, Cx43 and traces of Cx45, is used. Electrical recordings on microelectrodes are performed to characterize the cardiac conduction velocity (CV). The electrical activity was recorded before and after pacing at frequencies 2Hz, 5Hz, 10Hz and 30Hz to mimic the changing beating frequency in the healthy and diseased heart. We observed that the higher the frequency, the slower the CV. Interestingly, the conduction becomes disorganized at 10Hz, and chaotic and not homogeneous after burst stimulations (30Hz), similar to signals observed in patients. This suggests that gap junction channels adapt to the frequency to ensure a safe propagation, up to a threshold that alters their make-up and electrical properties. Ongoing experiments by SiRNA transfection on each connexin will be realized to determine their specific contribution in regulating the CV. The biochemical characterization and patch clamp recordings are ongoing to correlate the localization and the levels of expression of Cxs to the electrical properties of GJC and the changes of CV.