Eyeblink conditioning is a simple form of motor learning. Normal activity in the cerebellar cortex, cerebellar nuclei and inferior olive is necessary for its acquisition but activity in the cerebellar output pathways is not. So essential aspects of this motor memory must be stored within cerebellar circuitry. Post-training, reversible neural inactivations disrupt memory consolidation processes and they have dissociated cortical and nuclear function. Cortical inactivations prevent consolidation of eyeblink conditioning but nuclear inactivations do not, suggesting memory storage within the cerebellar cortex. Inactivations at different delays after conditioning indicate that consolidation processes begin around 1 hour after conditioning and are nearly complete within 2 hours. Learning-related changes in gene expression also give clues to the location and mechanisms of memory storage. There is a significant upregulation of G-substrate (GS) expression in cerebellar cortex during eyeblink conditioning. GS is a Purkinje cell specific substrate for PKG and its upregulation suggests an activation of the NO-PKG-GS signalling pathway in conditioning. This pathway is important in parallel fibre LTD and cortical infusions of a PKG inhibitor impair eyeblink conditioning, indicating that LTD and this behavioural learning may share common mechanisms. The implications of these findings for models of motor memory formation in the cerebellum will be discussed.