This study examines the effects of alterations in nitric oxide (NO) production on rabbit retinal function. NG-nitro-L-arginine (L-NA) and L-arginine (L-Arg) inhibited the light-evoked compound action potentials (CAPs) from the optic nerve, but not the electroretinogram (ERG), in a concentration-dependent manner, whereas D-arginine had no effect. L-Arg partially reversed the L-NA-induced inhibitory effect, and L-NA prevented the L-Arg-induced attenuation of the CAPs. Sodium nitroprusside reduced both the CAPs and the ERG, whilst potassium ferricyanide did not affect the CAPs, and potentiated the ERG. We conclude that, independent of the vasculature, endogenous NO modulates neurotransmission (i.e. light-evoked CAPs), but probably not phototransduction (i.e. light-evoked ERG) in this intact in vitro central nervous system preparation.