7th June, 2002 13:00:24 -0400 (Reuters Health)
By Jacqueline Stenson
NEW YORK (Reuters Health) - In a finding that could one day lead to new treatments for paralysis, stroke and other neurological disorders, researchers say they have gained new insight into why nerve cells of the brain and spinal cord do not repair themselves after injury.
In a series of laboratory experiments with rats, the investigators found that nerve cells, or neurons, of the brain and spine lost their ability to regenerate around the time the animals were born.
The brain and spine together are called the central nervous system. Nerves in the rest of the body are known as the peripheral nervous system. While peripheral neurons can regenerate, central nervous system neurons cannot.
"The embryonic (neurons) grew like gangbusters, but postnatal (just after birth) and adult neurons grew 10 times slower," said study author Dr. Ben A. Barres, a neurobiologist at Stanford Medical School in California.
Neurons are made up of a large cell body with an elongated "arm" called an axon that sends messages to other cells. The cells also have many branches known as dendrites that receive messages from other neurons. Nerve damage from injury or disease usually involves destruction of the axon, which then does not regenerate.
It's been known that a type of cell known as a glial cell in the central nervous system can inhibit the repair of damaged axons, and therapeutic efforts have been targeting this process.
But when the investigators separated glial cells from the neurons in the lab, they found that damaged adult neurons still lost their ability to properly regenerate, suggesting another mechanism was at play, according to the report in the June 7th issue of Science. The research involved neurons in the retina of the eye, a common model for studies of regeneration of the central nervous system.
With further experiments, the researchers found that amacrine cells--a type of nerve cell known as an interneuron--that are produced in the maturing retina around the time of birth appeared to trigger neurons to switch permanently from an axon-producing mode to a dendrite-producing mode.
The next step is to determine whether other interneurons elsewhere in the central nervous system have a similar affect on neurons in those areas, said Barres.
"With this finding, these investigators provide evidence that the poor growth of adult (central nervous system) axons is not simply a consequence of the local environment, but is a property acquired during development," Lisa McKerracher and Benjamin Ellezam of the University of Montreal in Quebec, Canada write in an editorial accompanying the study.
The findings offer hope that researchers may one day develop new treatments based on this process, they add.
"The challenge now will be to discover the signals that switch neurons back to the axon-growth mode," the editorialists write. The new work "suggests that a better understanding of the developmental switch from axonal to dendritic growth may hold the key to regeneration in the (central nervous system)," McKerracher and Ellezam point out.
"Not only are the central nervous system glial cells different from the peripheral nervous system glial cells, but the neurons are different too," Barres told Reuters Heath. "So we're going to have to address both aspects of this to help patients."
SOURCE: Science 2002;296:1860-1864.
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