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It was previously found that the efficacy of synaptic transmission between retinal cone systems and luminosity-typehorizontal cells (LHCs) was activity-dependent. Repetitive activation of red-cone pathway increased the LHC’s hyperpolarizingresponse to red light, and the response enhancement was reversible. In this study, intracellular recording and pharmacological methodwere applied to investigate the mechanism(s) underlying red-flickering-induced response enhancement. Lowering intracellular Ca2+ inthe LHC by intracellular injection of Ca2+ chelator EGTA prevented the development of red-flickering-induced response enhancement,which implicates the importance of postsynaptic calcium signal. The response enhancement could also be eliminated by a potentantagonist of Ca2+-permeable AMPA receptor (CP-AMPAR), which suggests the possibility that Ca2+ influx via glutamate-gatedcalcium channels is related to the changes of [Ca2+]i. Furthermore, the administration of ryanodine or caffeine also attenuated thephenomenon, which gives evidence that the local calcium signal caused by intracellular calcium-induced calcium release (CICR) may beinvolved. Taken together, our data implicate that postsynaptic CICR and CP-AMPAR are related to the activity-dependent responseenhancement.