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.