The tottering mouse, which harbors a mutation in the CACNA1A gene encoding a P/Q-type voltage-gated calcium channel, serves as a robust tool in neuroscience research for investigating Epilepsy and Episodic Ataxia Type 2 (EA2). In this study, we characterized the tottering mouse phenotype by leveraging ex vivo (loose-cell) and in vivo (extracellular) electrophysiology recordings of Purkinje cells (PCs) within the cerebellum, along with behavioral tests. Our findings reveal that tottering mice display increased irregularity in action potential (AP) firing of PCs without a change in frequency, but this effect was only seen in the absence of fast synaptic blockers (CNQX and picrotoxin). In vivo recordings in anesthetized mice also showed increased irregularity of AP firing in tottering mice. Behaviorally, tottering mice exhibited decreased locomotor activity in an open arena, reduced grip strength in the inverted mesh test, increased falls in the beam walk test, and reduced latency to fall in the rotarod test - all indications of reduced motor coordination and performance. Additionally, stressor and novel environment exposure resulted in higher disability scores in tottering mice. The present study shows that irregularity in the pacemaker activity of PCs positively correlates with deficits in motor tasks, which could underlie the decreased motor performance in the tottering model. Together, these results align with existing literature, emphasizing the tottering mouse’s suitability in preclinical research on EA2 mechanisms and for proof-of-concept of potential therapeutic strategies.