Abstract
Gap junctions provide direct cytoplasmic continuity between cells forming a low resistivity barrier to electrical propagation. As such, aberrant regulation of these low resistive conduits has been blamed for electrical conduction disorders in diseased myocardium. While there is a plethora of evidence that abnormalities in gap junctional communication underlie many forms of ventricular arrhythmias, the role of gap junctions in atrial conduction disorders has been less well studied. The atria are the most heterogeneous cardiac structures in terms of the gap junction proteins, connexins (Cx), which are present. Cx40 is the primary, or most abundant, gap junction protein in atria although Cx43 is also abundantly expressed. Cx45 is also expressed in atria, although at low levels. This heterogeneity in connexins leads to a complexity that makes understanding the role of cell coupling in conduction disorders and arrhythmogenesis difficult. In this review we focus on what is known about atrial connexins and their role in atrial fibrillation but also on the challenges presented in understanding the complex interplay between the individual connexin isoforms.