Cardiac fibroblasts are by number the largest component of the non-myocytes, providing structural support for the heart by regulating the synthesis and degradation of extracellular matrix components. Previous experimental studies suggested that there is electrical coupling between fibroblasts and cardiac myocytes (Gaudesius et al. 2003). The aim of this study was to use computational models to investigate the functional impacts of the electrical coupling between fibroblasts and myocytes on mouse atrial tissue vulnerability to the genesis of reentrant excitation waves. Based on extant voltage-clamp data on the kinetics and current densities of mouse atrial membrane ionic channels (INa, ICaL, INaCa, Ito, IK1, IKur, IKs) and intracellular Ca2+ dynamics, we developed a novel biophysically detailed mathematical model for simulating the electrical action potential of a mouse atrial cell. The model was validated by its ability to reproduce the experimentally measured physiological characteristics of a mouse atrial myocyte, including the resting potential, action potential amplitude, action potential duration and its rate-dependence). The developed atrial cell model was then coupled to a passive or an active fibroblast model (MacCannell et al. 2007) with one myocytes being coupled to one to ten fibroblasts. The coupled fibroblast-myocyte single cell model was then incorporated into 1D and 2D multi-cellular tissue models. Our simulation data suggested that at the single cell level, myocyte-fibroblast coupling elevates myocyte resting potential and prolongs its action potential duration (APD), which are monotonically increased with the increased number of fibroblasts. It enhances the supernormal excitability of atrial cells reflected by a larger APD at high pacing rates than at low pacing rates. At the 1D tissue level, the fibroblast-myocyte coupling reduces the conduction velocity of excitation waves, but reduced the width of a time window during which a premature stimulus may evoke unidirectional conductional block. At the 2D tissue level, regions of coupled fibroblast-myocytes disturb the excitation wavefront, leading to formation of re-entrant excitation wave in response to a series of rapid stimulus. In conclusion, the electrical coupling between fibroblast and myocytes disturbs cardiac conduction, facilitating the formation of re-entrant excitation wave that is pro-arrhythmic.