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Cannabinoid signaling system plays an important role in regulation of many neuronal functions in the CNS.Endocannabinoids function as a retrograde signaling to regulate the synaptic plasticity via activating presynaptic CB 1 receptors in many brain areas.To date, the effects of this signaling on synaptic transmission in retina are poorly understood.In the present study, we aimed to explore the modulation of cannabinoid signaling on glycinergic and GABAergic inhibitory inputs, and glutamatergic excitatory inputs to retinal ganglion cells (RGCs) by patch-clamp techniques in rat retinal slices.Our results show that activation of presynaptic CB 1 receptors in both GABAergic and glycinergic amacrine cells (ACs) suppressed the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in the RGCs through inhibiting the presynaptic voltage-gated calcium channels.Although the effect of cannabinoid on glutamatergic excitatory inputs from bipolar cells to the RGCs is basically similar, the tonic inhibitory inputs from the ACs to the bipolar cells are necessary.Blocking these inhibitory inputs eliminated completely the suppression effect of cannabinoid on the excitatory inputs to the RGCs.The underlying mechanism is that deinhibition-induced depolarization of bipolar cells inactivates the presynaptic T-type calcium channels that is a target of the activated presynaptic CB 1 receptors in the bipolar cells.Our data revealed a new mechanism of cannabinoid modulating synaptic transmission in the inner retina.