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High temporal resolution of vision relies on the rapid kinetics of the photoresponse in the light-sensing photoreceptor neurons.It is well known that the activation/deactivation of photoreceptor largely depends on the visual transduction cascades within photoreceptors.However,how photoreceptor neurons achieve the stable resting membrane potential is not clear.Here we show that Ih channels play an essential role in regulating photoreceptor cell activity through retinal-lamina microcircuit.We performed an ERG-based mutagenesis screen and isolated a mutant fly which exhibits ERG baseline oscillation in dark.Intracellular recording revealed that periodic activation of photoreceptors leads to ERG baseline oscillation in the mutant flies.We further indentified that Ih channels expressed in L1/2 lamina neurons and amacrine cells,but not in photoreceptors.Expression of Ih channel in amacrine cells was sufficient to inhibit ERG baseline oscillation in the mutant flies.We further demonstrated that Ih channel in amacrine cells was essential for the inhibition of glutamate synaptic release by suppressing the activity of low-threshold voltage-gated calcium channel.Finally,we screened the glutamate receptors in photoreceptor axons and identified kainite receptors that mediates the glutamatergic signaling from amacrine cells.Our studies indicated that a photoreceptor-amacrine cell feedback loop mediates the regulation of photoreceptor activity.