Retinal pathways involved in the control of eye growth and myopia

Abstract

AbstractPurpose To integrate information from studies on gene expression in animal mpdels and from genetic studies on human myopia to define the pathways which are involved in the development of myopiaMethods A literature search of studies on gene expression in animal models of myopia and human genetic studies was carried out using the Medline databaseResults Human genetic studies identify two clusters of mutations which are involved in human high myopia. One involves genes which affect photoreceptor and ON‐bipolar cell function in the outer retina. These mutations are associated with congenital stationary night blindness. A second cluster involves genes involved in extracellular matrix structure and function, which may be important in the sclera, which changes markedly during the development of myopia. ON‐bipolar cells play a major role in the control of dopamine release in the retina. Other evidence supports a role for dopamine in the control of eye growth, which suggests a plausible pathway linking the genes involved in the outer retina to control of eye growth. However, the down‐stream effects of changes in dpoamine release are not well‐characterised studies. However, animal studies have suggested that changes in the expression of the early intermediate gene ZENK and changes in glucagon release within the retina may play a roleConclusion Huamn genetic studies and studies of changes in gene expression in animal models of myopia provide a consistent but still incomplete picture of the pathways involved in the control of eye growth. Further studies on these pathways are of particular importance given that they implicate retinal dopamine release , which links them to the epidemiological evidence that bright light‐ induced dopamine release can prevent the development of myopia in humans