•  Early afterdepolarizations (EADs) are a known trigger for arrhythmias, but the effect of surrounding tissue on EADs is poorly understood. •  Neurotoxin anthopleurin‐A (AP‐A) increases action potential duration and gives rise to EADs in isolated myocytes. We investigate the effect of AP‐A on connected networks of cultured cardiac cells. •  We show that EADs are markedly suppressed in well‐coupled neonatal rat ventricular monolayers treated with AP‐A, but reappear when gap junction connectivity is blocked. •  The ability of cell coupling to electrotonically damp EADs is confirmed in a two‐cell simulation where connectivity is systematically varied. •  Taken together, these results suggest that cell–cell coupling can act to suppress EADs in normal cardiac tissue. Results also suggest that EADs may emerge and propagate in poorly coupled tissue. Abstract  Pathologies that result in early afterdepolarizations (EADs) are a known trigger for tachyarrhythmias, but the conditions that cause surrounding tissue to conduct or suppress EADs are poorly understood. Here we introduce a cell culture model of EAD propagation consisting of monolayers of cultured neonatal rat ventricular myocytes treated with anthopleurin‐A (AP‐A). AP‐A‐treated monolayers display a cycle length dependent prolongation of action potential duration (245 ms untreated, vs. 610 ms at 1 Hz and 1200 ms at 0.5 Hz for AP‐A‐treated monolayers). In contrast, isolated single cells treated with AP‐A develop prominent irregular oscillations with a frequency of 2.5 Hz, and a variable prolongation of the action potential duration of up to several seconds. To investigate whether electrotonic interactions between coupled cells modulates EAD formation, cell connectivity was reduced by RNA silencing gap junction Cx43. In contrast to well‐connected monolayers, gap junction silenced monolayers display bradycardia‐dependent plateau oscillations consistent with EADs. Further, simulations of a cell displaying EADs electrically connected to a cell with normal action potentials show a coupling strength‐dependent suppression of EADs consistent with the experimental results. These results suggest that electrotonic effects may play a critical role in EAD‐mediated arrhythmogenesis.