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News

Myelin suppresses plasticity in the mature brain

Yale University : 29 September, 2005  (New Product)
Yale School of Medicine researchers report in Science this week genetic evidence for the hypothesis that myelination, or formation of a protective sheath around a nerve fiber, consolidates neural circuitry by suppressing plasticity in the mature brain.
Yale School of Medicine researchers report in Science this week genetic evidence for the hypothesis that myelination, or formation of a protective sheath around a nerve fiber, consolidates neural circuitry by suppressing plasticity in the mature brain.

This finding has implications for research on restoring mobility to people who have lost motor functions due to spinal cord injury, multiple sclerosis, Lou Gehrig's disease, and other central nervous system disorders.

'The failure of surviving neurons to reestablish functional connection is most obvious after spinal cord injury, but limited nerve cell regeneration and plasticity is central to a range of neurological disorders, including stroke, head trauma, multiple sclerosis, and neurodegenerative disease,' said senior author Stephen Strittmatter, professor in the Departments of Neurology and Neurobiology. 'Recovery of motor function after serious damage to the mature brain is facilitated by structural and synaptic plasticity.'

Strittmatter's laboratory studies how myelin in the central nervous system physically limits axonal growth and regeneration after traumatic and ischemic injury, when blood supply is cut off. A physiological role for the myelin inhibitor pathway has not been defined.

Blocking vision in one eye normally alters ocular dominance in the cortex of the brain only during a critical developmental period, or 20 to 32 days postnatal in mice. Strittmatter's lab, working in collaboration with Nigel Daw, M.D., professor of ophthalmology and neuroscience, and his group, found that mutations in the Nogo-66 receptor affect plasticity of ocular dominance. In mice with altered NgR, plasticity during the critical period is normal, but it continues abnormally so that ocular dominance later in development is similar to the plasticity of juvenile stages.
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