Bergmann glia (BG) are radial glial cells in the cerebellar cortex that have multiple functions. They have been shown to interact with Purkinje cells in several ways: they modulate synaptic inputs to Purkinje cells, regulate excitability through external potassium concentration, and directly affect Purkinje cells through neurotransmitter release. In this study, we genetically expressed hM3Dq in BGs through GFAP-promoter-contained AAV virus. We showed that this BG-PC regulation is mediated by the NMDA receptor and GABAA receptor. Furthermore, using calcium imaging, we confirmed that BG activation induces MLI activation. Taken together, we concluded that glutamate released from BG induces GABA release from MLI, which in turn inhibits PC activity. Our findings provide a cellular mechanism for understanding the role of BG in the modulation of neuronal activity in the cerebellum.​​​​