The research, reported in the Dec. 14 issue of Current Biology, overturns the long-standing belief that blindness from chronic light exposure is a direct result of overall retinal degeneration and cell death.
Although many animals, and presumably humans, lose both their retinal cells and vision after exposure to low levels of light for long periods, the relationship between exposure and blindness had been poorly understood.
In the Hopkins experiments, flies whose light-detecting protein rhodopsin was engineered to resist destruction retained their vision twice as long as normal flies, although over time they developed blindness due to delayed decay of rhodopsin. The researchers measured vision damage indirectly by measuring loss of the electrical signals normally initiated by rhodopsin when exposed to light.
"Everyone assumed that the blindness caused by chronic light exposure was an effect of the degeneration and loss of the retinal cells, but our experiments show these are two distinct events caused by two distinct processes," says Craig Montell, Ph.D., professor of biological chemistry in Hopkins' Institute for Basic Biomedical Sciences. "Understanding how degradation of rhodopsin and other visual proteins contributes to vision loss may help us in the future to reduce the severity of blindness in rare people susceptible to chronic exposure to light."
The light-detecting cells of fruit fly retinas share similarities with rod and cone cells of the human retina and also rely on rhodopsin to detect light and create an electrical signal that is transmitted to the brain.