Using patch clamp techniques, we characterized glycine-induced currents from cones in bullfrog retinal slices. Application of glycine to cone terminals induced an inward current, which was in part suppressed by strychnine. The remaining strychnine-resistant current component, which did not show polarity reversion in a range of -120 mV to +40 mV, was blocked by N[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl] sarcosine, an antagonist of glycine transporter 1 (GlyT1), but not affected by amoxapine, an inhibitor of glycine transporter 2. Application of sarcosine, an agonist of GlyT1, to cone terminals induced an inward current that was completely suppressed by N[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl] sarcosine or when external Na in Ringer's was replaced by choline. All these results show for the first time the functional expression of GlyT1 on bullfrog cones.