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 Research & Giving News Article  The presumed distinction between white matter and grey matter has long been one of the staples of knowledge about the mammalian brain. “White matter” is white because of the presence of myelin, the fatty substance that in healthy brains surrounds axons, or nerve fibers. This fatty insulation allows electrical signals to be transmitted rapidly over long distances. “Grey matter” contains the main body of nerve cells, or neurons. The new discovery, made in mouse cells, was reported in the cover story of the March issue of Nature Neuroscience. It indicates that brain cells “talk” with each other in more ways than previously thought. “We were surprised to see these nerve axons ‘talking’ to other cells in the white matter,” said Dwight Bergles, Ph.D., an associate professor of neuroscience at Hopkins and a 2005 NARSAD Young Investigator. The discovery focuses on oligodendrocyte precursor cells (OPCs). OPCs are immature versions of a class of glial cells, or support cells, in the brain called oligodendrocytes that are responsible for producing the myelin that sheaths nerve fibers. The immature OPC cells simply hang around and divide very slowly, waiting to be spurred into action. To learn more about OPCs that reside in the brain’s white matter, Dr. Bergles and his Johns Hopkins colleagues measured activity from individual precursor cells in the corpus callosum, a region of white matter that connects the two brain hemispheres. To their surprise, OPCs were found to have electrical signals produced by the neurotransmitter glutamate. These signals were similar to the signals central in cell-to-cell communication and information processing in the gray matter. The phenomenon was unlikely, the scientists said, because in the mouse brain, OPCs in the myelin-rich white matter are far from synapses, the junctions between nerve cells where glutamate is released. Theorizing that OPCs might have engaged glutamate in some less obvious way in this area of the brain, Dr. Bergles and his team studied nearby nerve cells to figure out where the glutamate might be coming from. By inducing individual neurons to become excited one at a time, they discovered that as electrical impulses were carried along their axonal projections, glutamate was released. This, in turn, generated electrical signals in OPCs. A further microscopic hunt revealed that pools of glutamate were present in the nerve fibers wherever they touched OPCs. All of the nerve cells in the white matter that released glutamate within reach of OPCs, moreover, had something in common: no myelin insulation. Normally myelin speeds electrical impulses. Cells lacking the coating fire 20 to 90 times slower than cells coated with myelin. Myelin loss is well known to impair signaling and information processing, causing nerve cells to die and creating such neurodegenerative conditions as multiple sclerosis. Dr. Bergles speculates that this white matter activity may help “naked” nerve cells signal nearby OPCs and say “cover me with myelin because we need to replace another cell that has been damaged.” The finding may have implications for serious mental illness. Existing studies have indicated that people with schizophrenia exhibit a decrease in myelin in the prefrontal cortex, a decrease in expression of myelin-associated genes, and a decrease in the density of mature oligodendrocytes. These facts suggest that death or dysfunction of these cells may contribute to the behavioral changes seen in the disease. The dearth of oligodendrocytes in schizophrenia specifically suggests that OPC differentiation may be interrupted. Dr. Bergles’ studies of signaling in the brain ultimately may provide new insights not only into schizophrenia, but also the mechanisms responsible for the beneficial effects of antidepressive therapy. |
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