Intracellular recordings of oscillatory firing (bursting activity) were obtained from Purkinje cells (PCs) in rat cerebellar slices. Apamin inhibited post-burst hyperpolarizations (PBHs) progressively and finally terminated oscillatory firing activity of PCs. Apamin did not affect the amplitude or duration of the after-hyperpolarization (AHP) between spikes within the burst. In the voltage clamp mode, apamin shifted the whole-cell, quasi-steady state I/V relationship in an inward direction and abolished the zero slope resistance (ZSR) region by blocking outward current. Nickel (Ni2⁢) terminated oscillatory activity and also abolished the ZSR region. However, Ni2⁢ did not have progressive blocking action on the post-burst hyperpolarization before it blocked oscillatory activity. Ni2⁢ blocked an inward current at potentials positive to approximately ⁣65 mV, which was responsible for the ZSR region and outward current at more negative potentials. These data indicated that oscillatory activity of PCs is sustained by a balance between a slow Ni2⁢-sensitive inward current and an apamin-sensitive outward current in the region of ZSR of the whole-cell I/V curve.