While studies of cerebellar involvement in learning and memory have described plasticity within the cerebellum, its role in acquisition of plasticity elsewhere in the CNS is largely unexplored. This study set out to determine whether the cerebellum is needed for acquisition of the spinal cord plasticity that underlies operantly conditioned decrease in the H-reflex, the electrical analog of the spinal stretch reflex. Rats in which the cerebellar output nuclei dentate and interpositus (DIN) had been ablated were exposed for 50 d to the H-reflex down-conditioning protocol. DIN ablation, which in itself had no significant long-term effect on H-reflex size, entirely prevented acquisition of a smaller H-reflex. Since previous studies show that corticospinal tract (CST) transection also prevents down-conditioning while transection of the rubrospinal tract and other major descending tracts does not, this result implies that DIN output that affects cortex is essential for generation of the CST activity that induces the spinal cord plasticity, which is, in turn, directly responsible for the smaller H-reflex. The result extends the role of the cerebellum in learning and memory to include participation in induction of plasticity elsewhere in the CNS, specifically in the spinal cord. The cerebellum might simply support processes in sensorimotor cortex or elsewhere that change the spinal cord, or the cerebellum itself might undergo plasticity similar to that occurring with vestibulo-ocular reflex (VOR) or eyeblink conditioning. Activity-dependent plasticity, which is now known to occur throughout the CNS and through a variety of mechanisms, is presumed to underlie learning. However, the mechanistic relationships between this plasticity and learned behavioral changes remain largely obscure. The complexity and limited accessibility of the CNS, combined with the fact that even simple learning involves plasticity at multiple sites (Wolpaw and Lee 1989;Carrier et al. 1997;Cohen et al. 1997;Lieb and Frost 1997;Thompson et al. 1997;Whalen and Pearson 1997;Lisberger 1998;Garcia et al. 1999;Medina et al. 2000Medina et al. , 2002Hansel et al. 2001;King et al. 2001;Wolpaw and Tennissen 2001;Carey and Lisberger 2002; van Alphen and De Zeeuw 2002;Blazquez et al. 2003), makes it hard to trace the connections from specific experiences to specific occurrences of activity-dependent plasticity, and thence to specific behavioral changes (Wolpaw 2002). Efforts to do so use experimental models based on simple behaviors produced by defined and accessible neural circuitry.Two of these models, vestibulo-ocular reflex (VOR) plasticity and eyelid conditioning, reveal plasticity in the cerebellum and associated brainstem nuclei that underlies relatively rapid behavioral change (Kim and