Retinal Control of Eye Growth and Myopia

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The eye and vision are critical to survival, and adaptation to changing conditions is essential for sensing form, contrast, and movement. The long-term goals of our studies are to identify the specific nerve cells, neural circuits, and chemical messengers involved in retinal adaptation to changing lighting conditions, and to identify the retinal systems that can cause or prevent myopia.We will test the idea that light-adaptation activates retinal networks and functional pathways utilizing the transmitters dopamine (DA), nitric oxide (NO), and acetylcholine (ACh), and that these pathways act together to regulate ocular growth and prevent myopia, under these themes:1. Temporal modulation of light intensity as the effective stimulus for moving spatial patterns.Interruption of form-deprivation by 2-3 hrs of normal viewing prevents experimentally induced "form-deprivation" myopia. We predict that this is due to flickering of light, as textured images move across the retina, and that the key retinal pathways prevent myopia via DA, NO, or ACh receptors.2. Prevention of myopia by antagonists to muscarinic acetylcholine receptors (mAChR).Some muscarinic antagonists, such as atropine, prevent myopia in chicks and mammals, but unacceptable side-effects limit their therapeutic use for human myopia. Identifying the specific receptor through which atropine prevents myopia will be helpful in the development of better anti-myopia drugs.3. Retinal mechanisms of spatiotemporal processing and contrast discrimination.Using the optokinetic reflex (head-turning to follow a drifting stripe pattern) and the induction/prevention of form-deprivation myopia as indicators of retinal circuit function, we will determine how DA, NO, and ACh contribute to adaptation in retinal circuits. The resulting discoveries will reveal basic visual mechanisms that are at work in the retinas of most vertebrate species, including those of humans, and may yield new therapies for myopia.