This paper reviews results that support a model in which memory for VOR gain is initially encoded in the flocculus, and in which cerebellar LTD and LTP are responsible for gain increases and gain decreases, respectively. We also review data suggesting that after it is encoded, motor memory can either be disrupted, possibly by a local mechanism, or else consolidated. We show that consolidation can be rapid, in which case the frequency dependence of learning is unchanged and we will argue that this is consistent with a local mechanism of consolidation. In the longer term, however, the available evidence supports the transfer of memory out of the flocculus. In new experiments reported here, we address the mechanism of memory encoding. Pharmacological evidence shows that both mGluR1 and GABA(B) receptors in the flocculus are necessary for gain-up, but not for gain-down learning. Immunohistochemical experiments show that the two receptors are largely segregated on different dendritic spines on Purkinje cells. Together with what is already known of the mechanisms of cerebellar LTD and LTP, our data suggest that the direction of learning may be determined by interactions among groups of spines. Our results also provide new evidence for the existence of frequency channels for vestibular signals within the cerebellar cortex.