Summary T-type Ca 2+ channel family includes three subunits Ca V3.1, Ca V3.2 and Ca V3.3 and have been shown to control burst firing and intracellular Ca 2+ concentration ([Ca 2+] i) in neurons. Here, we investigated whether Ca V3.1 channels could generate a pacemaker current and contribute to cell excitability. Ca V3.1 clones were over-expressed in the neuronal cell line NG108-15. Ca V3.1 channel expression induced repetitive action potentials, generating spontaneous membrane potential oscillations (MPOs) and concomitant [Ca 2+] i oscillations. These oscillations were inhibited by T-type channels antagonists and were present only if the membrane potential was around −61 mV. [Ca 2+] i oscillations were critically dependent on Ca 2+ influx through Ca V3.1 channels and did not involve Ca 2+ release from the endoplasmic reticulum. The waveform and frequency of the MPOs are constrained by electrophysiological properties of the Ca V3.1 channels. The trigger of the oscillations was the Ca V3.1 window current. This current induced continuous [Ca 2+] i increase at −60 mV that depolarized the cells and triggered MPOs. Shifting the Ca V3.1 window current potential range by increasing the external Ca 2+ concentration resulted in a corresponding shift of the MPOs threshold. The hyperpolarization-activated cation current ( I h) was not required to induce MPOs, but when expressed together with Ca V3.1 channels, it broadened the membrane potential range over which MPOs were observed. Overall, the data demonstrate that the Ca V3.1 window current is critical in triggering intrinsic electrical and [Ca 2+] i oscillations.