According to research published online today in Nature, the team from Imperial College London and the University of Manchester, have discovered that activating the melanopsin gene in the nerve cells causes them to become light responsive, or photoreceptive.
Using mouse cells, the researchers found that melanopsin could be used to make neurones light responsive. They found that as well as being sensitive to blue light, melanopsin uses light at different wavelengths to regenerate itself. In some forms of hereditary blindness photoreceptors are lost entirely, but the retinal ganglion cells, the cells which signal to the brain, remain intact. The researchers believe that by activating the melanopsin, these cells may gain the ability to sense and respond to light.
Professor Mark Hankins, from Imperial College London and Charing Cross Hospital, and one of the papers authors, comments: "It is quite remarkable that the activation of a single gene can create a functional photoreceptor. It is an important proof of principle that melanopsin can make non-light sensitive cells receptive to light, and although not a cure, could have applications in treating some forms of blindness."
Dr Rob Lucas, from the University of Manchester, and one of the paper's authors, adds: "The discovery that melanopsin is capable of making cells photosensitive has given us a unique opportunity to study the characteristics of this interesting protein. The textbook view of the eye is that it contains only two light sensing systems, the rods and cones. However, over the last few years it has become increasingly accepted that we have a third system, which uses melanopsin, that has lain undetected during decades of vigorous scientific investigation."
Professor Hankins and Dr Lucas were part of the team who previously discovered a new light detection system in the eye, totally independent of the rods and cones, which were thought to be the only systems providing sight. They measured light-induced pupillary constriction in genetically modified mice that lacked melanopsin. When the mice lacking melanopsin were exposed to low light, their pupillary response was the same as normal mice, but when they were exposed to bright light their pupil constriction was incomplete.
The researchers believe that while not a cure for blindness, the findings could lead to therapies for treating some forms of blindness, such as retinitis pigmentosa. Retinitis pigmentosa is a form of hereditary blindness where the rods and cones are destroyed, but the rest of the eye and retina remains intact. By switching on the melanopsin it could be possible to restore the eyes ability to respond to light.
Although making cells in the eye responsive to light is not a cure for blindness, the team are collaborating with engineers from Imperial to develop a functional retinal prosthesis which would allow the information from the light responsive cells to be used by the brain to process images.
The research was supported by a Wellcome Trust Showcase Award and the BBSRC.
Journal
Nature