Nitric oxide, 2-amino-4-phosphonobutyric acid and light/dark adaptation modulate short-wavelength-sensitive synaptic transmission to retinal horizontal cells.

Light-induced changes in the input resistance (Rin) of external, luminosity (i.e. H1) type horizontal cell (HC) perikarya were studied by the bridge-balance method in light-adapted and dark-adapted retinae of carp. Changes in input resistance (delta Rin) induced by short-(460 nm) and long-wavelength (674 nm) flashes, adjusted in intensity to elicit equal-amplitude membrane voltage responses (equal-voltage condition), were measured. In light-adapted retinae, long-wavelength stimuli increased Rin consistently; in contrast, the increase was much less with short-wavelength stimuli. This equal-voltage chromatic delta Rin difference was lost in dark-adapted retinae whereby the delta Rin (an increase) became the same for short- and long-wavelengths. The chromatic delta Rin difference could be recovered by light adaptation or application of sodium nitroprusside to the dark-adapted retinae. Conversely, the equal-voltage chromatic delta Rin difference was eliminated by injection of NG-monomethyl-L-arginine into H1HCs of the light-adapted retinae or by treating the retinae with 2-amino-4-phosphonobutyrate (APB). These results suggest that H1HCs of the carp retina possess distinct postsynaptic mechanisms which mediate short- and long-wavelength signal transmission. Furthermore, it appears that the short-wavelength-sensitive pathway is active only during the light-adapted state of the retina. Taken together, therefore, the short-wavelength transmission to H1HCs probably operates on an APB-sensitive glutamate receptor, with nitric oxide as a light-adaptive messenger.