Slice across the human brain, and you'll see tracts of white matter glistening against dull gray matter. The latter contains bodies of nerve cells, which help us fill out tax forms, fall in love and learn the rules of baseball. White matter, on the other hand, contains the long arms or axons of these neurons. The axons cable messages across the brain and down the spinal cord, instructing us to move a pen, kiss a lover or hit a home run.
Stroke and head trauma can rob us of the means to think and act by killing parts of the brain. Studies of how such events damage gray matter have flourished in recent years, and drugs to reduce nerve cell loss now are in clinical trials. But scientists have paid scant attention to loss of white matter, which increases long-term disability, deprives spinal cord patients of bowel and bladder control and can account for most symptoms of multiple sclerosis.
Cells called oligodendrocytes make white matter white. They manufacture myelin, the fatty sheath that insulates axons like plastic around an electrical wire. If their myelin falls into disrepair, axons cease to function, even though they themselves aren't damaged. So protecting oligodendrocytes after brain or spinal cord injury might keep intact axons in action.
A chance observation led researchers at Washington University School of Medicine in St. Louis to discover how oligodendrocytes might die after catastrophes in the central nervous system and how this loss might be prevented. John W. McDonald, M.D., Ph.D., and Mark P. Goldberg, M.D., assistant professors of neurology, and Dennis W. Choi, M.D., Ph.D., the Jones Professor and head of neurology, discovered that oligodendrocytes succumb to elevated levels of a brain chemical called glutamate, an observation that flies in the face of previous dogma. They presented their findings in the March 1998 issue of Nature Medicine.