Researchers have identified a molecule capable of regenerating damaged nerves in the spinal cord. Their finding is reported in today's issue of Neuron.
Nerve cells in the spinal cord don't heal in the same way as bone and tissue do. A well-known case in point is the actor Christopher Reeve, whose 1995 fracture to the spinal column left him with no movement below the neck.
Until recently, many scientists believed that damage to these nerve cells could not be repaired. However, a puzzling experiment with laboratory rats appeared to suggest that regeneration could occur, at least under certain circumstances.
Certain nerve cells have two branches. One of these branches goes to our limbs while the other goes into the spinal cord. As expected, a lesion to the latter cannot normally be repaired. However, researchers had observed that if the limb branch was cut prior to damaging the spinal cord branch, this branch could re-grow soon after injury. Their suspicion was that this “peripheral” injury was generating some signal that traveled to the spinal cord and would help it regenerate.
Three research teams have now found that a molecule called “cAMP” mediates this signal. Research teams led by Marie Filbin at Hunter College and Marc Tessier-Lavigne and Allan Basbaum at Stanford/UCSF found that if rats were injected with cAMP prior to the lesion (as a substitute for the peripheral injury) this was sufficient to induce re-growth of nerves following injury. Remarkably, a single dose of cAMP was able to produce this effect.
Building on previous studies using cultured neurons, these researchers also showed that cAMP acts by changing the intrinsic growth properties of the neurons themselves.
Neurons treated with cAMP were able to regenerate in culture even in the presence of molecules that normally inhibit their growth. Since it is thought that the presence of such inhibitory molecules in the injured spinal cord contributes to the lack of regeneration following injury, it is possible that treatment of injured neurons with cAMP may be a way of overcoming this inhibitory effect. So, rather than removing these inhibitory molecules entirely, neurons can be coaxed to respond to them differently.
“Because the treatment is not at the lesion site, it raises the possibility of developing a therapy that does not require intervention directly at the site of injury, which could result in even more damage,” said Filbin.
[Contact: Marie T. Filbin, Allan I. Basbaum, Marc Tessier-Lavigne]
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