Abstract
Optic nerve hypoplasia is seen in 50% of patients diagnosed with fetal alcohol syndrome and is due to a defect in the development of retinal ganglion cells. Somatostatin may influence the development of retinal ganglion cells, so we studied the effect of in vivo ethanol exposure on somatostatin expression in the developing retina. Somatostatin concentration is increased in retina from ethanol-exposed fetuses and pups and this increase in peptide is associated with excessive neurite formation and improper migration of the somatostatin-containing neurons at early postnatal ages. These disturbances may account for the eventual failure in retinal ganglion cell development that results in optic nerve hypoplasia.
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