Gap junction channels, composed of connexin subunit proteins, are involved in electrical impulse propagation and coordinated contraction of the heart. Out of 20 connexin (Cx) genes in the mouse genome, only Cx40, Cx45 and most recently Cx30.2 (Kreuzberg et al., Circ Res. 96: 1166–1177, 2005) were reported to be expressed in the cardiac conduction system, whereas Cx43 is mainly expressed in working cardiomyocytes. The corresponding connexin null (KO) mice show right bundle branch block Cx40KO), reduced conduction velocity (conditional Cx43KO) or embryonic lethality due to morphological defects in cardiac and vascular development (Cx45KO). Using new conditional Cx45KO mice (Cx45flox/flox:alpha MHC-Cre), we have recently found that the P-wave and AV conduction are prolonged, suggesting a slow-down of conduction velocity. Furthermore, new Cx30.2 deficient mice show a 25% shorter PQ interval and a 25% accelerated conduction in the AV node (collaboration with J. Schrickel, A. Ghanem, T. Lewalter, and K. Tiemann, Med. Klinik II, Universität Bonn). Thus, the deceleration of impulse propagation in the AV node of wild type mice, where Cx30.2 is abundantly expressed, could be due to the very low unitary conductance (9 pS) measured for Cx30.2 channels in transfected HeLa cells. Cx30.2 channels are likely to be involved in coordination of atrial to ventricular contraction and protection towards pathophysiological states.