Long-term depression (LTD) of excitatory transmission at cerebellar parallel fibre-Purkinje cell synapses is a form of synaptic plasticity crucial for cerebellar motor learning. Around the postsynaptic membrane of these synapses, B-type gamma-aminobutyric acid receptor (GABA_BR), a G_i/o protein-coupled receptor for the inhibitory transmitter GABA, is concentrated and closely associated with type-1 metabotropic glutamate receptors (mGluR1) whose signalling is a key factor for inducing LTD. We found that in cultured Purkinje cells, GABA_BR activation enhanced LTD of a glutamate-evoked current (LTD_glu), increasing the magnitude of depression. It has been reported that parallel fibre-Purkinje cell synapses receive a micromolar level of GABA spilt over from the synaptic terminals of the neighbouring GABAergic interneurons. This level of GABA was able to enhance LTD_glu. Our pharmacological analyses revealed that the subunits but not the subunit of G_i/o protein mediated GABA_BR-mediated LTD_glu enhancement. G_i/o protein activation was sufficient to enhance LTD_glu. In this respect, LTD_glu enhancement is clearly distinguished from the previously reported GABA_BR-mediated augmentation of an mGluR1-coupled slow excitatory postsynaptic potential. Baclofen application for only the induction period of LTD_glu was sufficient to enhance LTD_glu, suggesting that GABA_BR signalling may modulate mechanisms underlying LTD_glu induction. Baclofen augmented mGluR1-coupled Ca²⁺ release from the intracellular stores in a G_i/o protein-dependent manner. Therefore, GABA_BR-mediated LTD_glu enhancement is likely to result from augmentation of mGluR1 signalling. Furthermore, pharmacological inhibition of GABA_BR reduced the magnitude of LTD at parallel fibre-Purkinje cell synapses in cerebellar slices. These findings demonstrate a novel mechanism that would facilitate cerebellar motor learning.