Abstract

We have tracked the structural and functional development of normal retina and used these normative data to facilitate interpretation of the retinal dysfunction and dysmorphia associated with retinopathy of prematurity (ROP). ROP, a potentially blinding disease, is active when the neurosensory retina is quite immature. Interpretation of non-invasive psychophysical and electrophysiological data in infants and children and in rat models of ROP are backed up by our biophysical, molecular biological, and histological data in the rats. A key result is that the onset of active ROP coincides with development of the rod photoreceptor outer segments and the phototransduction cascade. Dysfunction of the rods persists for years after the active disease has healed in early infancy. Taken all together, our results lead us to propose light as a non-invasive, non-pharmacological intervention designed to minimize and ultimately prevent ROP and its consequences.

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