Noradrenaline (NA) modulates synaptic transmission in various sites of the central nervous system. In the cerebellar cortex, several studies have revealed that NA enhances inhibitory synaptic transmission via -adrenoceptor- and cyclic AMP-dependent pathways. However, the effects of -adrenoceptor activation on cerebellar inhibitory neurotransmission have not yet been fully understood. Therefore, we investigated the effects of the ₁- or ₂-adrenoceptor agonist on inhibitory postsynaptic currents (IPSCs) recorded from mouse Purkinje cells (PCs). We found that the non-selective -adrenoceptor agonist 6-fluoro-norepinephrine increased both the frequency and amplitude of spontaneous IPSCs (sIPSCs). This enhancement was mostly mimicked by the selective ₁-adrenoceptor agonist phenylephrine (PE). PE also enhanced the amplitude of evoked IPSCs (eIPSCs) and increased the frequency but not the amplitude of miniature IPSCs (mIPSCs). Moreover, PE decreased the paired-pulse ratio of eIPSCs and did not change GABA receptor sensitivity in PCs. Conversely, the selective ₂-adrenoceptor agonist clonidine significantly reduced both the frequency and the amplitude of sIPSCs. Neither eIPSCs nor mIPSCs were affected by clonidine. Furthermore, presynaptic cell-attached recordings showed that spontaneous activity of GABAergic interneurons was enhanced by PE, while reduced by clonidine. These results suggest that NA enhances inhibitory neurotransmitter release via ₁-adrenoceptors, which are expressed in presynaptic terminals and somatodendritic domains, whereas suppresses the excitability of interneurons via ₂-adrenoceptors, which are expressed in presynaptic somatodendritic domains. Thus, cerebellar -adrenoceptors play roles in a presynaptic dual modulation of GABAergic inputs from interneurons to PCs, thereby providing a likely mechanism for the fine tuning of information flow in the cerebellar cortex.