A sudden car accident, an on-the-job injury or a freak skiing collision can all cause irreparable damage to the delicate neuronal axons that wire the human central nervous system. Axons are extensions of nerve cells that transmit electrical signals. Once injured, they are incapable of regaining functionality, which often inflicts paralysis and numbness on the victim. Current thinking brands an assortment of inhibitory agents, including central nervous system cells called glial cells, that surround the damaged neurons as culprits for this failure to regrow. Research published today in the journal Science, however, challenges this basic assumption. The findings suggest that adult nerve cells permanently lose the ability to grow new axons after making contact with another type of nerve cell known as amacrine cells. According to the report, once this contact is made, the axons permanently switch to the next stage in their developmental cycle.

Using the rat retina as a simple model for the central nervous system, Jeffrey L. Goldberg of the Stanford University School of Medicine and his colleagues tested both neurons from rat embryos and cells from more mature animals. Examined under an identical battery of favorable environmental conditions, the embryonic cells consistently extended their axons 10 times as fast as the older cells did, leading the team to conclude that something other than environmental cues slowed the growth of the mature cells. At some point, it seemed, these older neurons lost their intrinsic ability to grow axons at all. Further tests showed that an external signal, provided through contact with amacrine cells, caused this change. The scientists propose that the amacrine cells acted by somehow flipping a permanent developmental switch in the maturing neuron: instead of devoting further energy to axonal growth, the neuron started to grow dendrites, which receive electrical signals. Once a neuron has been switched from axonal to dendritic growth, the team reports, it can never go back.

To repair devastating injuries to the central nervous system, damaged neurons need to be returned to a state of axon growth. The new findings provide an important first look into how that might occur and offer insight into what may be the key behind neuronal regeneration.