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Eye’s light-detection system revealed


A research team led by Johns Hopkins scientists has discovered that a special, tiny group of cells at the back of the eye help tell the brain how much light there is, causing the pupil to get bigger or smaller. The findings, which appeared in the Jan. 10 issue of Science, largely complete the picture of how light levels are detected in the eye.

"This tiny group of cells, together with rods and cones, are the bulk of the eye’s mechanisms for detecting levels of light and passing that information to the brain," says King-Wai Yau, Ph.D., professor of neuroscience and a Howard Hughes Medical Institute investigator at the Johns Hopkins School of Medicine.

The team previously had shown that this set of retinal cells, all of which contain a protein called melanopsin, are naturally sensitive to light. They also showed that the cells connect to the brain in such a way that they are poised to control how the pupil reacts to light and how animals adapt to day and night.

The new work proves that these melanopsin-containing cells, a subset of so-called retinal ganglion cells, are in fact a working part of the body’s light-detection system and complement the light-detecting role of rods and cones, which also convey information about the color, shape and movement of objects.

"Rods and cones provide high sensitivity to light, allowing the pupil to constrict, but melanopsin-containing cells seem to be crucial for completing the pupil’s response in bright light," says Samer Hattar, Ph.D., a postdoctoral fellow in neuroscience at Johns Hopkins. "Without melanopsin, the pupil fails to constrict fully, even in very bright light."

First authors Hattar and Robert Lucas, Ph.D., of the Imperial College, London, measured how small the pupil of each of two kinds of "knockout" mice became when exposed to known amounts of light. One set of mice were missing the gene for the melanopsin protein, the others lacked rods and cones. In mice without melanopsin, only rods and cones send light to the brain, and in mice without rods and cones, only retinal ganglion cells do so.

In normal mice, the pupil becomes the size of a pinhole when exposed to very bright light. The pupils of "rod-less/cone-less" mice got just as small, but in mice without melanopsin, the smallest attainable size was three times larger than in other mice, the researchers found.

Importantly, they also proved that, even without melanopsin, retinal ganglion cells still develop and connect to the brain in the same way, underscoring that the decreased pupil response is due to melanopsin’s absence.

"In the olfactory system, knocking out certain proteins changes the way the system is wired to the brain, and that easily could have been the case here," says Yau. "Melanopsin is clearly involved in light detection in these retinal ganglion cells, but it is not crucial for their development or connectivity."

At this point the scientists can’t rule out a third contributor in the eye’s light detection system, but report that combining the responses of the two sets of knockout mice matches the pupil response of normal mice very well. "Any other factor in detecting light is of minor importance, at least for the pupil reflex," says Yau.

The U.S. researchers were funded by the National Eye Institute and the Howard Hughes Medical Institute. The researchers in England were funded by the U.K. Biotechnology and Biological Sciences Research Council and Hammersmith Hospital Special Trustees. Authors on the paper are Hattar and Yau of Johns Hopkins; Lucas and Russell Foster of the Imperial College, London; and Motoharu Takao and David Berson of Brown University.

Johns Hopkins Medical Institutions’ news releases are available on an EMBARGOED basis on EurekAlert at and from the Office of Communications and Public Affairs’ direct e-mail news release service. To enroll, call 410-955-4288 or send e-mail to

Joanna Downer | EurekAlert!
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