These new cells could detect incoming light and network with other cells in the eye to relay signals to the brain, a potential step toward reversing certain genetic eye conditions and injuries. “Nobody more than me wants this to be true,” says Seth Blackshaw, a neuroscientist at Johns Hopkins University’s School of Medicine in Baltimore, Maryland, “but I have serious concerns about this study.” The Müller glia in fish and amphibian eyes can divide and specialize into cells that replace damaged or lost neurons. But mammalian eyes don’t spontaneously repair themselves like that. In this case Müller glia don’t seem to regenerate neurons except after an injury.
Bo Chen, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York City, and his colleagues hoped to restore photoreceptors without damaging the eye. “We’re trying to wake up the self-repair mechanisms that we know are happening in zebrafish,” he says. In the experiment, Müller glia targeted by gene-carrying viruses generated cells that were rodlike in their structure and in signaling ability. However, their density was just 0.2% of what you’d expect in a healthy retina. The treated mice probably perceived light, but they couldn’t make out shapes or objects. Chen and his team are now exploring other genes that might drive Müller glia.