New Haven, Conn.-Yale School of Medicine researchers report inScience this week genetic evidence for the hypothesis that myelination,or formation of a protective sheath around a nerve fiber, consolidatesneural circuitry by suppressing plasticity in the mature brain.
This finding has implications for research on restoring mobility topeople who have lost motor functions due to spinal cord injury,multiple sclerosis, Lou Gehrig's disease, and other central nervoussystem disorders.
"The failure of surviving neurons to reestablish functionalconnection is most obvious after spinal cord injury, but limited nervecell regeneration and plasticity is central to a range of neurologicaldisorders, including stroke, head trauma, multiple sclerosis, andneurodegenerative disease," said senior author Stephen Strittmatter,professor in the Departments of Neurology and Neurobiology. "Recoveryof motor function after serious damage to the mature brain isfacilitated by structural and synaptic plasticity."
Strittmatter's laboratory studies how myelin in the centralnervous system physically limits axonal growth and regeneration aftertraumatic and ischemic injury, when blood supply is cut off. Aphysiological role for the myelin inhibitor pathway has not beendefined.
Blocking vision in one eye normally alters ocular dominance inthe cortex of the brain only during a critical developmental period, or20 to 32 days postnatal in mice. Strittmatter's lab, working incollaboration with Nigel Daw, M.D., professor of ophthalmology andneuroscience, and his group, found that mutations in the Nogo-66receptor (NgR) affect plasticity of ocular dominance. In mice withaltered NgR, plasticity during the critical period is normal, but itcontinues abnormally so that ocular dominance later in development issimilar to the plasticity of juvenile stages.
Science (September 30, 2005)
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