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S. G. Crewther, M. J. Murphy Edwards, S. Scott, M. J. Goodyear, S. N. Kiely, D. P. Crewther; A Neuromodulatory Explanation for the Effects on Refractive Compensation of Nitric Oxide. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3673.
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© ARVO (1962-2015); The Authors (2016-present)
Nitric oxide (NO) has been associated with many ocular responses including flicker modulation of retinal ON pathway activation, choroidal expansion and refractive compensation to optical blur. Thus this study aimed to clarify whether the effects of modulation of retinal NO [by nitric oxide synthase (NOS) inhibitor L-NAME or the NOS substrate L-Arginine (L-Arg),] on refractive compensation to optical defocus, of retinal NO [by nitric oxide synthase (NOS) inhibitor L-NAME or the NOS substrate L-Arginine (L-Arg),] could be better explained by altered balance of the activation of the ON/OFF pathways or changes in choroidal thickness.
Biometrics, ERGs (at 2 and 4 days) and histology were examined after rearing chicks from day 5-9 with monocular lenses (+/-10D, No Lens), single intravitreal injections of L-NAME, L-Arginine or Saline and under standard diurnal (SD) or low frequency ramped flicker (LFRF) luminance conditions. Fellow eyes were injected with saline.
Single intravitreal injections of both drugs continued to enhance the ERG ON/OFF (b/d) wave amplitude ratios for 4 days but did not affect refractive compensation to +10D lens and No Lens wearing eyes but did significantly inhibit compensation to -10D and choroidal thickness under standard diurnal (SD) light conditions. Under LFRF, refractive compensation to +10D lens was suppressed while compensation to -10D groups was enhanced with no differences in choroidal thickness for either lens or drug groups.
Thus the results indicate that under the SD conditions, ERG b/d wave-amplitudes ratios are better predictors of the direction of relative refractive compensation than are choroidal thickness measurements and suggest that any longer term changes in neuromodulatory function induced by the NOS perturbing drugs are more important to refractive compensation than transiently induced vasomotor effects.
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