Fast (approximately 160 Hz) cerebellar oscillation has been recently described in different models of ataxic mice, such as mice lacking calcium-binding proteins and in a mouse model of Angelman syndrome. Among them, calretinin-calbindin double knockout mice constitute the best model for evaluating fast oscillations in vivo. The cerebellum of these mice may present long-lasting episodes of very strong and stable local field potential oscillation alternating with the normal non-oscillating state. Spontaneous firing of the Purkinje cells in wild type and double knockout mice largely differs. Indeed, the Purkinje cell firing of the oscillating mutant is characterized by an increased rate and rhythmicity and by the emergence of synchronicity along the parallel fiber axis. To better understand the driving role played by these different parameters on fast cerebellar oscillation, we simultaneously recorded Purkinje cells and local field potential during the induction of general anesthesia by ketamine or pentobarbitone. Both drugs significantly increased Purkinje cell rhythmicity in the absence of oscillation, but they did not lead to Purkinje cell synchronization or to the emergence of fast oscillation. During fast oscillation episodes, ketamine abolished Purkinje cell synchronicity and inhibited fast oscillation. In contrast, pentobarbitone facilitated fast oscillation, induced and increased Purkinje cell synchronicity. We propose that fast cerebellar oscillation is due to the synchronous rhythmic firing of Purkinje cell populations and is facilitated by positive feedback whereby the oscillating field further phase-locks recruited Purkinje cells onto the same rhythmic firing pattern.