PURPOSE. It has been shown that sunlight or bright indoor light can inhibit the development of deprivation myopia in chicks. It remains unclear whether light merely acts on deprivation myopia or, more generally, modulates the rate of emmetropization and its set point. This study was conducted to test how bright light interacts with compensation for imposed optical defocus. Furthermore, a dopamine antagonist was applied to test whether the protective effect of light is mediated by dopamine. METHODS. Experiment A: Chicks monocularly wore either -7 or +7 D lenses for a period of 5 days, either under normal laboratory illuminance (500 lux, n = 12 and 16, respectively) or under high ambient illuminance (15,000 lux, n = 12 and 16). Experiment B: Chicks wore diffusers for a period of 4 days, either under normal laboratory illuminance (500 lux, n = 9) or high ambient illuminance (15,000 lux), with the bright-light group intravitreally injected daily with either the dopamine D2 antagonist spiperone (500 μM, n = 9) or a vehicle solution (0.1% ascorbic acid, n = 9), with an untreated group serving as the control (n = 6). Axial length and refraction were measured at the commencement and cessation of all treatments. RESULTS. Exposure to high illuminances (15,000 lux) for 5 hours per day significantly slowed compensation for negative lenses, compared with that seen under 500 lux, although full compensation was still achieved. Compensation for positive lenses was accelerated by exposure to high illuminances but, again, the end point refraction was unchanged, compared with that of the 500-lux group. High illuminance also reduced deprivation myopia by roughly 60%, compared with that seen under 500 lux. This protective effect was abolished, however, by the daily injection of spiperone, but was unaffected by the injection of a vehicle solution. CONCLUSIONS. High illuminance levels reduce the rate of compensation for negative lenses and enhance the rate for positive lenses, but do not change the set point of emmetropization (target refraction). The retardation of myopia development by light is partially mediated by dopamine, as the injection of a dopamine antagonist abolishes the protective effect of light, at least in the case of deprivation myopia.