Sept. 26, 2018
A new study in mice hints at how night vision works, and provides clues to how the visually impaired could be helped, Emily Underwood writes in Science.
The study revealed that motion-sensing nerve cells in the retina temporarily change how they wire to each other in dark conditions. The findings might one day help visually impaired humans, Underwood writes.
To find out how direction-selective ganglion cells (DSGCs) in mammalian eyes adapt to the dark, neuroscientist Greg Field and colleagues at Duke University in Durham, North Carolina, examined slices of mouse retinas by laying them on tiny glass plates embedded with an electrode array. Each array includes about 500 electrodes, but is so small that it spans just a half-millimeter, Field told Underwood. Bathed in an oxygenated solution, the mouse retinas can still function and “see” while the array records electrical activity from hundreds of neurons.
The team showed the dissected retinas a simple movie—bands moving across a contrasting background—then turned the light down by a factor of 10,000, going from typical office-level lighting to a more moonlit scene. Three of the four directional DSGCs remained “rock solid” in their response to the motion when the lights went down, Field explained to Underwood. But the fourth type, which usually responds to upward motion, now responded to a much broader range of motion, including down and sideways.
Field and his colleagues then analyzed why the “up” cells were acting oddly. Using a computer model of all four directional cells’ activity, they concluded that when the “up” cells sacrificed some of their preference for one direction, they improved the performance of the group as a whole, boosting DSGCs’ ability to detect motion in low light.
To find out how the “up cells” had switched their function, scientists genetically engineered mice that lacked intra-cellular connections called gap junctions in their up-sensing neurons. Such protein channels allow chemical signals to pass from one neuron to another, and have previously been linked to night vision. Field’s team found that in retinal tissue from mice without the gap junctions, up-sensing cells didn’t adapt to the dark. That means that at least some of the “up” cells’ ability to boost motion detection in low light depends on gap junctions.
Whether this holds true in people as well is unclear, but the rodent insight might still be applied to artificial vision efforts, Underwood writes. Even though DSGCs make up just 4 percent of ganglion cells in humans, compared with about 20 percent in mice, many new retinal prosthetics for visually impaired people rely in large part on electrically stimulating ganglion cells. Studies like this could help fine-tune those technologies, Field told Underwood: “If you’re going to stimulate ganglion cells, you need to get them to send the right signals to the brain.”
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