Recently, under the leadership of the Stanford University School of Medicine, researchers have successfully repaired some of the key optic nerves of mammals for the first time. The study was published on the online website of the journal Nature Neuroscience. The scientists allowed the mouse's optic nerve (which is responsible for transmitting visual information from the eye to the brain) to successfully regenerate after being completely severed, and found that the optic nerve can re-track the previous path and re-establish contact with the appropriate parts of the brain. This unprecedented restoration work can help the blind to see the light again. Before the scientists reconstructed the optic nerve of the mouse, the symptoms of the mouse were similar to those of human glaucoma, which was the second most common cause of blindness other than cataract. Andrew Huberman, a senior author of the study and associate professor of neurobiology, points out that cataracts can usually be removed surgically, but glaucoma has no effective treatment. The lead author of the study was Jung-Hwan Albert Lim, a graduate student at the University of California, San Diego. Glaucoma is caused by excessive optic nerve pressure, and nearly 70 million people worldwide suffer from this disease. Trauma, retinal detachment, pituitary tumors, multiple brain cancers, and other causes can also cause damage to the optic nerve, leading to decreased vision. The retina is made up of a thin layer of cells that is no more than half the thickness of the credit card and is responsible for the light in the eye. If the nerve cells are in the office, this thin layer of tissue is like the bustling Manhattan. Photoreceptor cells in the posterior retina respond to different wavelengths of light by sending electrically encoded information to retinal ganglion cells. There are up to 30 types of retinal ganglion cells, each of which is good at handling different visual information, such as upward movement, overall movement, or red. Retinal ganglion cells have long, wire-like protrusions that are first bundled together, extending together to the optic nerve, and then emanate to various parts of the brain, connecting with other nerve cells, and transmitting visual information to them. "The brain can crack these electrical signals in some way, such as 'a car coming over there, I better retreat to the sidewalk'". Humberman said. “More than a third of the brain's area is used to process visual information,†he said. “More than 24% of brain regions are able to directly receive signals from retinal ganglion cells. These areas are not only related to what we usually think of. Regionally related, it is also related to day and night rules and emotions." Hubertman pointed out that retinal ganglion cells are the only cells that connect the eye to the brain. “When these cell axons are cut, it's like pulling the visually controlled plug out of the socket directly,†he added. When the brain and spinal cell axons of mammals such as mice and humans are damaged, they cannot recover by themselves. (The only known exception is the olfactory nerve cell.) Hubertman points out that the retina is also part of the brain, so once a mammalian retinal ganglion cell axon is damaged, it causes permanent vision loss. However, mammalian cell axons located outside the central nervous system are self-regenerating. In addition, in the early stages of human growth, cranial nerve cells and spinal nerve cells thrive, and axons can try to break through a pile of brain tissue that is in the middle of the road and reach farther. In fully mature adults, axons from retinal ganglion cells to superior colliculus can be as long as 6 to 8 inches (about 15 to 20 cm).
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