In order to maintain communication at the synapse, synaptic vesicles must be retrieved and recycled by endocytosis. At least two distinct mechanisms of vesicle retrieval exist; fast endocytosis and slow endocytosis. The mechanism of slow endocytosis is currently poorly understood, but it is known that strong stimulation is needed to trigger this pathway. Slow synaptic vesicle endocytosis is controlled by cyclin-dependent kinase 5 in an activity dependent manner. We have characterised this slow endocytic pathway in cerebellar granule neurons in order to determine the molecular mechanisms of this pathway. To do this we have determined the strength of stimulus required to activate slow endocytosis. We have investigated how these vesicles replenish the readily releaseable pool and the reserve pool. We have also looked at the essential molecular players in this process by overexpression and use of dominant negative mutants. These studies have highlighted the importance of the slow endocytic pathway in normal physiological function at the nerve terminal.