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Ever wonder why nerves don’t break when your body stretches? Traditional research model proposes “neurofilaments” provide the strength and flexibility for nerve cells.

But scientists have discovered a new protein that explains why a long nerve doesn’t break upon stretching.

Beta spectrin protein stops nerve cells from breaking.

Nerve cell stretchiness uncovered

US scientists may have discovered why long nerve cells do not break when you move or stretch your limbs.
Experiments in worms showed that when a protein called beta spectrin is missing, nerve cells are brittle and break, leading to paralysis.

The finding may help to explain why people with a condition called spinocerebellar ataxia progressively lose co-ordination and movement.

The University of Utah study is in the Journal of Cell Biology.

Humans have four genes responsible for the production of beta spectrin protein.

Recent studies have shown that people with a condition called spinocerebellar ataxia type 5, a neurodegenerative disease that develops between the ages of 10 and 68, have a mutation in one of the genes.

It was previously thought that the mutation in this protein meant cells could not communicate properly because the necessary proteins would not be anchored in place.

But research by Professor Michael Bastiani and colleagues at the University of Utah suggests that a mutation in or absence of the protein causes long nerve fibres (axons) to lose their flexibility and break.

When nematode worms were bred without beta spectrin their nerve axons died over time and caused paralysis.

In worm embryos only 3% of nerve cells were broken or defective but that grew to 60% by the time the worms were a day old, suggesting the protein is not responsible for initial growth of nerve cells but for preventing breakage later on.

Nerve function

Professor Bastiani said the team found it “incredible” that the one protein was responsible for preventing nerves breaking in your whole body.

“The entire functioning of the nervous system depends on these wire-like axons between nerve cells,” he said.

He added that when the worms were paralysed by a second mutation the nerve axons did not break because the worms were not moving around.

“What was surprising was in the past, it’s always been embedded in the literature that the thing that provides the strength and flexibility was the neurofilaments.

“We’re proposing a completely different model.”

Read more: bbc.co.uk

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