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AIM: To investigate the effect of DSX, an active component extracted from Erigeron breviscapus, on the voltage-gated outward K+channel currents in rat retinal ganglion cells(RGCs) by using electrophysiological method, and to explore the possible mechanisms of DSX on optic nerve protection.· METHODS: Outward K + currents were recorded by using whole-cell patch-clamp techniques on acutely isolated rat RGCs. Outward K+currents were induced by a series of depolarizing voltage pulses from a holding potential of-70 m V to +20 m V in an increment of 10 m V.·RESULTS: Extracellular application of DSX voltage-dependently suppressed both the steady-state and peak current amplitudes of outward K+currents in rat RGCs.Furthermore, DSX reversibly and dose-dependently inhibited the amplitudes of outward K+currents of the cells. At +20 m V membrane potential DSX at the concentrations of 0.02 g/L and 0.05 g/L showed no significant effects on the currents. In contrast, DSX at higher concentrations(0.1 g/L, 0.2 g/L and 0.5 g/L)significantly suppressed the current amplitudes.· CONCLUSION: These results suggest that DSX reversibly and dose-dependently suppress outward K+channel currents in rat RGCs, which may be one of the possible mechanisms underlying Erigeron breviscapus prevents vision loss and RGC damage caused by glaucoma.