91av

STRETCHING neurons on the rack might seem like torture, but it could be the
key to repairing spinal cords.

By gradually pulling apart bunches of neurons, Douglas Smith and his
colleagues at the University of Pennsylvania in Philadelphia have persuaded the
cells’ processes, or axons, to grow up to a centimetre in just 10 days. “For an
axon just a micron wide, that’s an enormous distance,” Smith says.

The researchers say these nerve cells could be used to bridge the gap between
damaged nerves in the spinal cords of people who are paralysed. They have
already begun trials in animals. “You can think about what we have as jumper
cables,” Smith says.

While it’s too early to know if the approach will work for people with spinal
cord injuries, Smith thinks it is a viable alternative to other strategies. For
example, many researchers are trying to encourage nerve cells to regrow in the
spine by, say, implanting an artificial scaffold seeded with appropriate
chemicals.

“But everything about the spinal cord is screaming ‘stop growing’,” Smith
says, so it’s hard to get axons to grow long distances. “The difference with
growing cells outside the body is that you don’t have to worry about this
inhibitory environment.”

Smith’s team placed groups of human neurons on adjacent membranes and grew
them for three days to allow the axons from the groups to form connections. The
membranes were then pulled apart 3.5 micrometres every 5 minutes over 10 days,
until the axons connecting the two groups of cells had grown a centimetre. Any
faster and the axons were torn apart. They ended up with long bundles containing
tens of thousands of axons.

It’s an interesting approach, says Paul Reier, a pioneering researcher into
spinal cord repair at the University of Florida. The big problem will be
implanting the cells in the right place and keeping them alive, he says. “Adult
neurons usually die when transplanted.”

But Smith says his team is using a cell line that managed to survive when
implanted into stroke patients. He also speculates that transplanting integrated
bundles of cells will boost their survival. “Cells may be less likely to die if
they stay with their ‘friends’,” he says.

Reier thinks it will someday be possible to persuade cells to grow long
distances in the spinal cord, though. “Axon growth is becoming less of a
challenge than we thought.”

Whatever approach is used, many questions remain. It’s not even clear that
bridging a damaged part of the spinal cord will restore nerve activity. In some
injuries, some or all of the nerve fibres remain intact, yet still don’t work,
Reier points out.

Smith’s work may also help us understand other disorders, however. He thinks
that stretch-induced growth plays an important role in embryos and children.
Some degenerative disorders in young children may be caused by nerve fibres that
can’t grow fast enough to keep up. Smith’s team is now trying to understand
exactly how the process works. “Nobody’s ever studied this type of growth
before,” he says.