What happens if the axon is damaged

During this extended period of excitability, PT and retraining can help guide injured neurons along beneficial pathways. But the injury-induced excitability in a neuron may cause problems too.

A neuron can die from overexcitement neuroscientists call this excitotoxicity. Neuronal hyperactivity after injury also may lead to intractable pain, muscle spasms, or agitation in the patient. In the days immediately after injury, doctors often treat brain-injury patients with drugs such as gabapentin designed specifically to suppress neuronal hyper-excitability. What scientists haven't understood very well are the biological details, the hows and whys of dendrite spine loss and hyper-excitability.

Those details have been elusive because of the spaghetti-like complexity of the brain, which makes it extremely difficult for a scientist to isolate a neuron and its axon for manipulation and analysis, either in a lab dish or a lab animal. Several years ago, as a biomedical engineering graduate student at the University of California-Irvine, Taylor invented a device to help solve this problem.

It's a microfluidic chamber with tiny grooves that trap individual axons from cultured neurons as they grow longer. Taylor and her colleagues used the device in the new study to analyze what happens when an axon is severed. They found that events within the neuron itself drive the resulting dendrite spine loss and hyper-excitability.

Signals originating at the site of injury move rapidly back along the remaining portion of the axon to the neuronal soma and nucleus, triggering a new pattern of gene activity. Taylor's team managed to block the neuron's gene activity to prevent the dendritic spine loss and hyper-excitability. Taylor and colleagues analyzed how gene activity changed before and after axotomy. Multiple genes were altered following axotomy.

The activity for one of these genes, encoding a protein called netrin-1, turned out to be sharply reduced. A separate analysis showed a similar drop in netrin-1 in affected neurons in rats whose axons from the brain to the spinal cord had been cut. Together, these results hinted that netrin-1's absence might be a major factor driving neuronal changes after axotomy.

When Taylor and colleagues added netrin-1 to axotomized neurons to restore the protein to normal levels -- even two full days after severing the axon -- they found that the treatment quickly reversed all of the dendritic spine loss and most of the hyper-excitability.

She added, "We're a long way off, but we really do hope to translate this netrin-1 finding into a new therapy. Ideally, it would do what gabapentin and related head-injury drugs aim to do, only better and more precisely. Each neuron in your brain has one long cable that snakes away from the main part of the cell. This cable, several times thinner than a human hair, is called an axon, and it is where electrical impulses from the neuron travel away to be received by other neurons.

Depending on the type of neuron, axons greatly vary in length - many are just a millimetre or so, but the longest ones, such as those that go from the brain down the spinal cord, can extend for more than a metre.

An axon typically develops side branches called axon collaterals, so that one neuron can send information to several others. These collaterals, just like the roots of a tree, split into smaller extensions called terminal branches. Each of these has a synaptic terminal on the tip.

Neurons communicate through synapses - contact points between the axon terminals on one side and dendrites or cell bodies on the other. Here, in a nanometre-wide gap, electrical signals coming via the axon are converted into chemical signals through the release of neurotransmitters, and then promptly converted back into electricity as information moves from neuron to neuron. Myelin acts as a form of insulation for axons, helping to send their signals over long distances.

For this reason, myelin is mostly found in neurons that connect different brain regions, rather than in the neurons whose axons remain in the local region. When this kind of damage affects peripheral nerves , symptoms of peripheral neuropathy can occur. Symptoms can vary depending on the type of nerve affected: motor, sensory or autonomic. Electrical impulses that pass along motor nerves, stimulate your muscles to move.

This permits people to do activities like walking or moving their fingers. Motor nerve damage can lead to muscle weakness, difficulty walking or climbing stairs and muscle cramps. Just like when your domestic electrical network is damaged and you call the electrician as soon as possible, even more for your nerves early diagnosis and the appropriate treatment are crucial to maintain your nervous system healthy.

The axon is a long, wire-like extension of the neuron that carries the signals from the cell body to other cells — such as nearby neurons or muscle cells.

Certain axons, such as those ones in the peripheral nervous system , can be wrapped in a substance called myelin that protects the nerve fibers and helps the rapid transmission of signals.