Brussels, 31 Jan 2005
A team of researchers from Imperial College London and the University of Manchester has discovered how to make eye cells light receptive, opening the way to a potential cure for certain forms of blindness.
The scientists found that activating the gene melanopsin in cells that do not normally use it made them sensitive to light and able to produce a biological signal.
'It is quite remarkable that the activation of a single gene can create a functional photoreceptor,' said Mark Hankins from Imperial College London.
'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,' added the University of Manchester's Rob Lucas.
Vision depends on the ability of rod and cone receptors in the retina to interpret light levels. Blindness is often caused by a disease of the retina in which these photoreceptors are destroyed.
Working with mice, the London-Manchester team found that turning on a gene for melanopsin caused nerve cells to work like photoreceptors.
'This discovery might provide food for thought for scientists looking for ways of treating visual loss,' explained Dr Lucas.
Making cells in the eye respond to light is not a cure for blindness but the researchers are working with medical engineers on prosthetic retinas that will help people with sight disorders to see more clearly. The melanopsin genes could also be inserted into intact cells in diseased retinas, turning them into functional photoreceptors. Although it is extremely unlikely that it would ever lead to fully restored sight, the discovery will probably lead to being able to restore black and white light sensitivity.
Experts believe this discovery could also provide new insights into sleep, insomnia, depression and seasonal affective disorder.
Item source: http:///dbs.cordis.lu/cgi-bin/srchidadb?C ALLER=NHP_EN_NEWS&ACTION=D&SESSION=&RCN= EN_RCN_ID:235