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Nature Medicine 9, 1347 - 1348 (2003)
doi:10.1038/nm1103-1347
Muscles flex, axons die
Jean R Wrathall1
- Jean R. Wrathall is in the Department of Neuroscience, Georgetown University Medical Center, Washington, D.C., 20057, USA. e-mail: wrathalj@georgetown.edu
Abstract
Molecules that regulate contraction in skeletal muscle have now found a place in the axon. In response to injury, the ryanodine receptor mediates the release of internal calcium stores, which contributes to axonal damage.
Axonal injury disconnects nerve cells from their targets and disrupts the sophisticated information network of the central nervous system (CNS). The injury can result from direct mechanical damage or reduced blood flow after events like stroke or trauma, and has long been known to involve accumulation of calcium within the injured axon1.
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