At parallel fiber-Purkinje neuron excitatory synapses, coupled activation of parallel fibers and a climbing fiber depresses the transmission for long-term. This phenomenon is called long-term depression (LTD), and it has been regarded as a primary cellular mechanism for motor learning. However, normal motor learning under LTD-suppressed conditions has been reported, and contribution of other synaptic plasticity mechanisms to motor learning has been suggested. At inhibitory synapses on a Purkinje neuron climbing fiber activation induces long-term potentiation of GABAergic synaptic transmission, which is called rebound potentiation (RP). We thought that RP may contribute to motor learning together with LTD, because induction conditions, molecular machinery and effects on Purkinje neuron activity are somewhat similar between LTD and RP. Thus, we addressed functional significance of RP by generating transgenic mice, in which a peptide that inhibits binding of GABARAP protein to GABA_A receptor is expressed selectively in a Purkinje neuron. The transgenic mice showed abrogated RP and subnormal adaptation of vestibulo-ocular reflex (VOR), a type of motor learning. However, adaptation of another type of reflex eye movement, optokinetic response (OKR) appeared normal. These results indicate that RP is involved in a certain type of motor learning, and that regulation mechanisms of VOR and OKR adaptations may differ. We examined relation of VOR and OKR, and found that trainings to induce VOR adaptations also changes dynamic properties of OKR but not vice versa. Neuronal regulation mechanisms of VOR and OKR adaptation might be distinct.