Clark Kellogg/Waisman Communicat
Joseph Ma (left) and John Svaren discovered that Schwann cells (green, inset above) may play more than just a passive role in the nervous system.
Dr. John Svaren likes to tell people that he’s “a biochemist pretending to be a neuroscientist.”
The biochemistry professor has spent much of his career studying the biology of the nervous system, particularly myelin, a fatty substance that insulates nerve fibers and increases the speed of electrical impulses carried through nerves.
This combination of interests opened the door for the UW professor and his grad student, Joseph Ma, to identify an important genetic switch in helper cells.
Schwann cells, which make up protective myelin sheaths surrounding axons — the long fibers in which neural impulses travel from the central nervous system outward — have been thought to mostly take a passive role in the peripheral nervous system.
But Svaren and Ma have discovered that the cells actually take a very active role in cleaning up injured tissue and supporting axon regeneration.
“After an injury, they have to change their whole program,” Svaren says. “What’s novel about that is no one ever identified a switch like this, which is important for the nerve injury process and the regenerative process after that.”
Svaren and Ma looked at the role of a protein called polycomb as it relates to the Schwann cells and myelin in mice and rats.
“We thought that inhibiting this one epigenetic switch would devastate myelin,” Svaren says. “When we took away the function of it, we thought that everything would go to hell in a handbasket.”
But instead, the animals’ cell behavior did not change for the worse, which prompted the team to look a bit closer.
The cells were able to make things in the nervous system that are normally only made after an injury.
“That was kind of a surprise for us since we had a totally different expectation of the experiment. In a way, it was really good because if the nerves had been devastated, then we wouldn’t have been able to discern this very specific role in the reprogramming of Schwann cells.”
This discovery, published in the August Journal of Neuroscience, has a potential to one day aid people with neuropathies, diabetes, multiple sclerosis and other severe disorders that affect the nervous system.
“If we can identify steps to get the Schwann cells to reprogram themselves a little bit better, especially in older individuals who have an injury issue, then that would be the ultimate goal of this research.”
Prior to this study, Schwann cells were thought to serve two purposes: protect nerve cells and speed up nerve impulses.
Axons need protection, Svaren says, because they are so long and vulnerable. Depending on how tall a person is, a single-celled axon could be a meter long.
For perspective, Svaren offers this: If a single peripheral nerve in a person’s toe were scaled to one meter, the connecting axon would be the length of the 1,300 kilometer (800 miles) Alaska oil pipeline.
“So there has to be a robust process to maintain them over the course of a lifetime.”
The other role of Schwann cells is to keep nerve impulses moving through the body quickly and efficiently.
“So when you trip on the sidewalk and your impulse makes your leg fly out in front so you don’t land on your face, that’s really due to this fast transmission of nerve impulses.”
Without that myelin sheath, messages are sent to the brain much slower.
“In the periphery nerves, we have sensory axons that are not myelinated. And that’s why if you put your hand on a hot stove, you don’t recognize it right away.”
Svaren and Ma’s discovery is far from being tested in humans, but it is still something the scientists are proud of. “We’re hoping to build onto that into the future,” says Svaren.
