Spinal cord axon injury location determines neuron’s regenerative fate
Scientists at University of California, San Diego School of Medicine have reported a previously unappreciated phenomenon in which the location of injury within the spinal cord axon determines whether the neuron attempts to regenerate. The study, published in Neuron, demonstrates how advances in live-imaging techniques are revealing new insights into the body’s ability to respond to spinal cord injuries.
Binhai Zheng, Ariana Lorenzana and colleagues used a sophisticated optical imaging technique to visualise the spinal cord in living mouse models and examine the effects of axon injury location on degeneration and regeneration of the injured branch. They compared injuries just before and after an axon’s major branch point.
The researchers found that injury to the main axon, before a branch point, resulted in regeneration in 89 per cent of cases. Axons with both branches cut after a branch point regenerated in 67 per cent of cases. Regeneration occurred in the form of axon elongation, branching or both for at least five days after injury. In contrast, regeneration occurred in only 12 per cent of cases following cuts to just one of two axon branches after a major branch point.
“What we think is happening is that if an axon is injured in such a way that it still has some kind of connection, is still transmitting signals, the neuron can justify stabilisation, but not the energy it would take to either regenerate axon length or just kill the whole thing off,” said Zheng. “On the other hand, once both branches of an axon are cut and there’s no longer any connection or output, the neuron can justify the energy and resources to regenerate, even though that effort is largely futile in the central nervous system of an adult mammal.”
Source: Eurekalert
Reference
Lorenzana, A.O., Lee, J.K., Mui, M., et al. (2015) A surviving intact branch stabilizes remaining axon architecture after injury as revealed by in vivo imaging in the mouse spinal cord. Neuron 86(4), 947–954. doi: 10.1016/j.neuron.2015.03.061
