But that road has proved difficult. Last year in the same journal, the Rochester team led by Giger showed that while the nogo receptor does play a role in preventing spinal nerves from growing, it does not control the process outright. While nogo receptor activation can transiently stunt the growth of neurons, it is not required for chronic outgrowth inhibition of injured nerve cells.
Gigers team has found that in some areas of the brain, such as the hippocampus, the nogo receptor is at least 10 times more prevalent than in the spinal cord.
In the brain, Gigers team found that the nogo receptor wields broad influence over a process known as neuroplasticity, which describes how our brain cells change and adapt constantly to meet our needs. It can be thought of simply as the brains ability to rewire itself on the fly to meet the demands of an organism. The process explains why people are able to recover many of their abilities even after a traumatic brain injury or a stroke: Other brain cells pick up the work for the ones that have died.
Gigers team found that the nogo receptor plays an important role in changing the brain in two ways.
First, the molecule plays a completely unexpected role manipulating the strength of signals between brain cells in the synapses. A team led by Peter Shrager, Ph.D., professor of Neurobiology and Anatomy, made sophisticated measurements of the strengths of the signals as they passed from cell to cell in mice. They found that mutant mice with fewer nogo receptors than normal had stronger brain signaling, what scientists call long-term potentiation.
The molecule also affected tiny structures known as dendritic spines, crucial connectio
|Contact: Tom Rickey|
University of Rochester Medical Center