Skeletal muscle differentiation depends on calcium ions, but it is yet unclear whether calcium entry through voltage-dependent calcium channels (VDCCs) contributes to the myoblast fusion process. In this study, we investigate whether calcium influx through functional T-type VDCCs precedes and affects mouse satellite cell fusion. We report here on the properties and the role of the VDCCs expressed in differentiating mouse muscular cells using both the C2C12 cell line and primary cultures of satellite cells. We present electrophysiological and biochemical evidence demonstrating that T-type and L-type VDCCs are not present in C2C12 and primary cultures of mouse satellite cells prior to the fusion stage. Although mRNA for the T-type CaV3.2 subunit was detected in differentiated C2C12 cells, no T-type calcium currents could be recorded, while both T-type and L-type calcium currents were detected after the fusion process in primary cultures. In addition, chronic application of 30 μM nickel, known to inhibit T-type CaV3.2 channels, did not alter the fusion of C2C12 cells and mouse satellite cells in primary culture. Overall, the data indicate that, unlike in humans, CaV3.2 T-type calcium channels play no role in mouse satellite cell fusion.