Rebound potentiation (RP) is a plasticity that occurs at interneuronal-Purkinje cell (PC) synapses in the cerebellum. It is caused by PC depolarisation inducing a Ca2+ influx that triggers a long term potentiation of GABAergic transmission. Although protein phosphorylation has been implicated in RP, the precise protein kinases involved are not defined and little is known about the physiological profile of this plasticity. In this study, we have investigated the time profile of RP after PC depolarisation at different time points following the formation of the whole-cell configuration. We have also identified protein kinases that appear to mediate RP. Day 11-14 postnatal Purkinje cells in parasaggital slices were voltage-clamped at -70mV. RP was induced after 5 mins by depolarising the PC to 0mV for 100ms duration (8x) at 0.5Hz. The mIPSC amplitudes gradually increased reaching a plateau of 163 ± 9 % (mean ± sem; n = 7) after 10 mins. The RP persisted for up to 30 mins after initiation. However, the amplitude potentiation for RP and its time profile varied with an increase in the latency of PC depolarisation. At 12 mins, a peak RP (short-term RP; 154 ± 17 %), occurred rapidly within 1 min after the stimulus followed by a rapid decline to baseline, before the resumption of a slower phase of RP (long-term RP) reaching a potentiation of 152 ± 14 % after 30 mins. With longer stimulus latencies up to 20 mins, short-term RP was abolished leaving only the long-term RP. To investigate the role of protein kinases in RP, we applied a novel and highly specific CaMKII inhibitor, CaMKIINtide. At 500nM, intracellular dialysis with this peptide completely abolished RP which was activated by PC stimulation after a 5 min latency (mIPSC amplitude = 88 ± 8 % of control at 30 mins post-stimulation). By contrast, the short-term RP observed with 12 min stimulus latency was only reduced to 126 ± 7 % of control at t = 1 min post-stimulation). The role of protein tyrosine kinases was assessed using the inhibitor genistein. Using a 12 min stimulus latency, intracellular-application of 100μM genistein abolished long-term RP (99 ± 13 % of control), but only reduced the short-term RP to 127 ± 17 % compared to control). Co-application of CaMKIINtide and genistein did not inhibit short-term RP any further (92 ± 8 %). Finally, the non-specific kinase inhibitor staurosporine (10μM) also failed to completely block the short-term RP (120 ± 4 %). These results indicate that RP can be separated into both short- and long-term potentiations of inhibitory synaptic inhibition depending on the latency of the stimulus. Furthermore, although the long-term RP is dependent on protein phosphorylation, the short-term RP exhibits a component that is either phosphorylation independent or insensitive serine-threonine and tyrosine kinase inhibition.