In some forms of blindness, notably retinitis pigmentosa and macular degeneration, the loss of vision is caused by the death of the rod and cone cells that actually sense light; the rest of the eye and visual system remains largely intact. This allows electrode implants to activate the nerves that relay signals from the eye on towards the brain, providing some hope of restoring vision. Now, researchers have figured out a clever way to get rid of all the hardware. They've tested a light-sensitive chemical that sticks to proteins on nerve cells, and causes them to fire off a nerve signal in response to light. When it's injected into the eye of otherwise blind mice, the chemical restores some light sensitivity.
The chemical in question is called AAQ (short for acrylamide-azobenzene-quaternary ammonium), and its activity on nerve cells was first described in 2008. In one of AAQ's forms, it binds to a protein that lets potassium ions into the cell, which makes nerve cells more likely to fire. In an alternate configuration, the molecule allows the ions to flow, causing nerve cells to shut down. The key feature of the molecule is that it's possible to switch AAQ between these two states using light: short wavelengths push it into the form that starts up potassium flow, while longer wavelengths cause it to switch back to shutting ion flows down.
To test whether this might work in the eye, the authors used mice that were engineered to carry mutations that cause the same defect that triggers retinitis pigmentosa in humans. (In addition, a second mutation knocked out an alternate pathway for sensing light.) Retinas obtained from these mice showed no response when exposed to light. But, once AAQ was added to them, there was a clear increase in activity when a light source was pointed at the retina.
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