Researchers at Wayne State University School of Medicine have managed to cause inner retinal neurons not normally sensitive to light, to respond to light through the introduction of a virus vector.
Using a harmless virus, they introduced a gene for a light-sensitive protein into “inner retinal neurons” in a strain of mice with photoreceptor deficiency that resembles the defect in such inherited human disorders as retinitis pigmentosa. Unlike the retinal rods and cones that normally function as light-sensing cells in the eye, these retinal neurons are normally not photosensitive. The light-sensitive protein they used, called channelrhodopsin-2 (ChR2), is found in green algae.
As reported in the April 6, 2006 issue of Neuron, Zhuo-Hua Pan of Wayne State University School of Medicine and colleagues found that the introduced protein rendered the retinal neurons sensitive to light. What’s more, they found, the protein persisted for long periods in the neurons, and the neurons generated signals that were transmitted to the visual cortex of the animals’ brains.
“With this strategy, the investigators have made a paradigm shift in the field and opened the possibility of genetically modifying the surviving retinal interneurons to function as a replacement light-sensing receptor,” wrote John Flannery and Kenneth Greenberg in a preview of the paper in the same issue of Neuron. “This publication is clearly a significant first step into this new field of re-engineering retinal interneurons as genetically modified ‘prosthetic’ cells,” they wrote.