Vision scientists at Washington University School of Medicine in St. Louis, U.S.A, have identified an intricate process that allows the human eye to adapt to darkness very quickly.The discovery could contribute to better understanding of human diseases that affect the retina, including age-related macular degeneration (AMD) as the disease and the pathway the researchers have identified both involve cone cells.
“AMD may be modulated, perhaps, through this pathway we’ve identified in the retina. Deficiencies in this pathway affect cone cells, and so does AMD, so it’s possible that if we could enhance activity in this pathway, we could prevent or reverse some of that damage to cone cells,” says principal investigator Dr Vladimir J. Kefalov.
The retina’s main light-sensing cells, rods and cones, both use similar mechanisms to convert light into vision, but they function differently. Rods are highly sensitive and work well in dim light, but they can quickly become saturated with light and stop responding. They don’t sense colour either, which is why we rarely see colours in dim light. Cones, on the other hand, allow us to see colours and can adapt quickly to stark changes in light intensity.
“The discovery could contribute to better understanding of human diseases that affect the retina…”
The researchers discovered that cone cells rely on light-sensing molecules that bind together to make up visual pigments. The pigments get destroyed when they absorb light and must be rebuilt, or recycled, for the cone cells to continue sensing light. After exposure to light, key components of pigments called chromophores can leave the cells and travel to the nearby pigment epithelium near the retina. There the chromophore is restored and returned to the photoreceptor cells.
Dr. Kefalov says exposure to bright light destroyed visual pigments in rods, and those cells could not recycle chromophores. Pigments in cones, by contrast, quickly regenerated and continued to detect light even without the pigment epithelium, so it was clear a second pathway was involved.
In the new study, Dr. Kefalov did the same experiments in cells from mice, primates and humans with the same result.
To learn how cones were able to recycle pigments without pigment epithelium, Kefalov’s team has focused on the Müller cells in the retina which support and interact with rods and cones. The researchers “blocked the function of Müller cells (in mice)” and discovered “the retinal visual pathway could not function because cones ran out of photopigment and could not adapt to dark,” Kefalov says. The new paper, published in the journal Current Biology, suggests Müller cells are key to this pathway in mammals, including humans.