The effect of nitric oxide synthase inhibitor on form-deprivation myopia

Form-deprivation myopia (FDM) is believed to result principally from actions of substances that modulate information processing in the retina. We used a chick model to investigate what role nitric oxide (NO), a gaseous neuromodulator, might play in the development of FDM.

We injected different concentrations of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) (30 ml) into the left eyes and the same volume of saline into the right eyes of 6-day-old chicks. Both eyes of most chicks were occluded for 6 days with translucent goggles. After removal of the goggles, the refraction was measured by retinoscopy and the axial lengths with an A-mode ultrasound. In some chicks we measured the concentration of NOx (nitrite and nitrate) in the retina. A few chicks, not wearing occluders after injection of L-NAME and saline, ERG and refraction, were examined 6 days after the treatment.

In chicks that wore occluders, refractive error and axial length were significantly less affected in eyes injected with L-NAME (180, 360, or 540 mM) compared to control (right) eyes. ERG changes were reversible, except in eyes injected with the highest concentration (540 mM) of L-NAME. The eyes of chicks, injected with L-NAME and reared without occlusion, had normal refractive values. After 6 days of form deprivation, the concentration of NOx in the retina of eyes injected with L-NAME (180 mM) was significantly less than the concentration in eyes injected with saline.

The injection of L-NAME before occlusion of developing chick eyes leads to reversible modifications in retinal function and inhibits the development of form-deprivation myopia.