How humans and other mammals could have their night vision | Science

On a moonless night, the light that reaches the Earth is a trillion times less than on a sunny day. However, most mammals still have a good chance of moving around, even without the special light-stimulating membranes in the eyes of cats and other nocturnal animals. A new study in mice suggests how this natural night vision works: nerve cells in the retina, which detect motion, temporarily change the way they fit into dark conditions. The results may one day help visually impaired humans, say the researchers.

Scientists already knew a little bit about how night vision works in rabbits, mice, humans and other mammals. Mammalian retinas can respond to a "ridiculously small" number of photons, says Joshua Singer, a University of Maryland neuroscientist at College Park who did not participate in the new study. A single photon can activate a light-sensitive cell called a stem cell in the retina, which sends an electrical signal to the brain through a ganglion cell.

A type of ganglion cell is specialized in motion detection – a vital function if you are a mouse driven by an owl or a person who launches to avoid oncoming traffic. Some of these selective ganglion cells of the direction (DSGC) are excited only when an object is moving upwards. Others shoot only when the objects move down or to the left or right. Together, the cells decide where an object is heading and pass this information to the brain, who decides how to act.

SGC says "DSGCs stand out as one of the few places in the brain" where neuroscientists feel confident enough that they know what neurons do. But the cells behave surprisingly when the lights go out.

To find out how DSGCs adapt to blackness, neuroscientist Greg Field and his colleagues at Duke University in Durham, North Carolina, examined slices of mouse retina by placing them on tiny glass plates. Each table includes about 500 electrodes, but it is so small that it only measures half a millimeter, says Field. Bathed in an oxygenated solution, mouse retinas can still function and "see" while the network records the electrical activity of hundreds of neurons.

The team showed the dissected retinas a simple film – bands moving over a contrasting background – then dropped the light by a factor of 10,000, rising from a typical office lighting to a more enlightened scene. Three of the four directional DSGCs remained "solid" in their response to motion when the lights went out, Field said. But the fourth type, which generally responds to the upward movement, now responds to a much wider range of movements, including up and down, they report today. neuron.

Field and his colleagues then analyzed why the "up" cells were acting strangely. Using a computer model of the activity of the four directional cells, they concluded that when "up" cells sacrificed some of their preferences for one direction, they improved the performance of the group as a whole light.

To find out how "cells at the top" have changed their function, scientists have genetically modified mice lacking intracellular connections called "gap junctions" in their stimulating neurons. Such protein channels allow chemical signals to pass from one neuron to another and have already been linked to night vision. Field's team found that in the retinal tissues of mice without gap junctions, the startled cells did not adapt to darkness. This means that at least some of the ability of "upward" cells to amplify motion detection in low light depends on gap junctions, say the authors.

It is unclear whether this is true in people, but rodent vision could still be applied to artificial vision efforts. Although DSGCs account for only 4% of ganglion cells in humans, compared to about 20% in mice, many new retinal prostheses for the visually impaired rely largely on electrically stimulating ganglion cells. Studies like this could help refine these technologies, says Field. "If you are going to stimulate ganglion cells, you have to get them to send the right signals to the brain."