Spontaneous excitatory postsynaptic currents (sEPSCs) were recorded under Whole-cell voltage clamp from carp type 1 horizontal cells (H1 cells) uncoupled by dopamine in retinal slices. Red light steps, which hyperpolarise cones and reduce glutamate release, induced outward current responses accompanied by a suppression of sEPSCs. sEPSCs decayed exponentially with a mean time constant of 0.71+/-0.07 ms and had a reversal potential near 0 mV. Power spectral analysis of sEPSCs revealed a similar decay time constant. They were suppressed by a non-NMDA receptor antagonist, CNQX at 10 μM, and a relatively specific AMPA receptor antagonist, GYKI52466 at 20 μM. The presence of sEPSCs suggests that the release of glutamate from cone synaptic terminals is vesicular. The reduction in mean sEPSC frequency with red light was not accompanied by a significant change in the mean sEPSC conductance increase (482+/-59 pS), suggesting that a decrease in the vesicular release rate from cones does not alter the vesicular glutamate concentration (quantal contents). The results suggest that the spontaneous events in H1 cells were contributed by non-NMDA (possibly AMPA) type glutamate receptors modulated by the red cone input.