Aims: The novel 1D Ca²⁺ channel together with 1C Ca²⁺ channel contribute to the L-type Ca²⁺ current (ICa-L) in the mouse supraventricular tissue. However its functional role in the heart is just emerging. We used 1D gene knockout (KO) mouse to investigate the electrophysiological features, the relative contribution of 1D Ca²⁺ channel to the global ICa-L, the intracellular Ca²⁺ transient, the Ca²⁺ handling by the sarcoplasmic reticulum (SR) and the inducibility of atrial fibrillation (AF). Methods and Results: In vivo and ex vivo ECG recordings from 1D KO mice demonstrated significant sinus bradycardia, atrio-ventricular block and vulnerability to AF. The wild-type mice showed no ECG abnormalities and no atrial fibrillation. Patch clamp recordings from isolated 1D KO atrial myocytes revealed a significant reduction of ICa-L (24.5%, P<0.05). However, there were no changes in other currents such as INa, ICa-T, IK, If and Ito and no changes in 1C mRNA levels of 1D KO atria. Fura-2 loaded atrial myocytes showed reduced intracellular Ca²⁺ transient (~40 %, P<0.05) and rapid caffeine application caused a 17% reduction of the SR Ca²⁺ content (P<0.05) and a 28% reduction (P<0.05) of fractional SR Ca²⁺ release in 1D KO atria. Conclusion: Genetic deletion of 1D Ca²⁺ channel in mice results in atrial electrocardiographic abnormalities and AF vulnerability. The electrical abnormalities in the 1D KO mice were associated with a decrease in the total ICa-L density, a reduction in intracellular Ca²⁺ transient and impaired intracellular Ca²⁺ handling. These findings provide new insights into the mechanism leading to atrial electrical dysfunction in the 1D KO mice.