PMCA2 is a fast, highly effective mechanism to control (by extrusion) resting cytosolic Ca²⁺ and Ca²⁺ excursions in neurones and other excitable cells. The strong expression of PMCA2 in the cerebellum and the cerebellar behavioural deficits presented by PMCA2-/- knockout mice all point to its importance for cerebellar circuit dynamics. AIM: to provide direct functional evidence for the influence of pre-synaptic PMCA2 mediated Ca²⁺ extrusion for short term plasticity at cerebellar parallel fibre to Purkinje neurone synapses. Whole cell patch clamp recordings from Purkinje neurones (PNs) within cerebellar slices from wild type (wt) and PMCA2-/- mice revealed enhanced paired pulse facilitation (PPF) of parallel fibre (PF) evoked EPSCs from PMCA2-/- PNs, that also took longer to return to baseline. Similar results were obtained in the presence of the PMCA inhibitor, carboxyeosin, but eosin was ineffective in PMCA2-/- cells. Additional results from intracellular Ca²⁺ measurements from bundles of pre-synaptic PFs showed that the decay of the PF Ca²⁺ transient was also enhanced in slices from PMCA2-/- slices compared with wt. Our results provide strong functional evidence for a contribution by PMCA2 to the clearance of Ca²⁺ from the PF pre-synaptic compartment to influence short term plasticity at the PF-PN synapse.