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Stanford explores new avenue for brain injury, paralysis research

ften die before regaining contact with other nerves. Most scientists blame this inability to regenerate on a group of nursemaid cells called glia, stationed around neurons. But Golderg's work suggests that while glia cells slow axon growth, they're not the only problem. Goldberg said that while neurons are developing, they get an outside signal they never forget. The message is: stop growing your axon so rapidly and start working on your dendrites.

To show that glial cells weren't solely responsible for the axon's slow regeneration, Goldberg removed the glia from axons in the optic nerves of embryonic and 8-day-old rats. (The optic nerve, which connects the brain to the eyeball, is an extension of the brain and is as injury-intolerant as the rest of the central nervous system.) Even without the glia, the embryonic neurons still regenerated 10 times faster than the neurons that developed in the 8-day-old rats.

From these results, Goldberg speculated that neurons had an internal clock that determined when they were destined to stop regenerating. To test his theory, Goldberg kept groups of isolated embryonic neurons alive in his laboratory until they were the same age as neurons in the 8-day-old rats. These lab-grown neurons were still able to regenerate axons quickly, while those taken from the recently born rats showed much slower axon growth.

These results told Goldberg that age was not the key to an axon's inability to regenerate. Rather, a signal that the neuron encountered in the developing rat must confer the "stop regenerating" message. Now, he had to find the culprit. "I asked if it was hormonal changes that happen at birth and found that it wasn't. So then I asked what kinds of cell types interact with the neurons," Goldberg said. At first he assumed the slow-down signal came from the site to which the axon grows. Upon researching that idea, he discovered instead that the signal was coming from the retina's intera
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Contact: Amy Adams
amyadams@stanford.edu
650-723-3900
Stanford University Medical Center
6-Jun-2002


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