Abstract

The cells that insulate neuronal processes with a myelin membrane sheath are damaged during stroke. Data now show that an influx of calcium ions mediated by the TRPA1 protein contributes to myelin injury. See Letter p.523 Fast nerve conduction relies on the insulating sheaths of myelin produced by glial cells — oligodendrocytes — of the white matter. These cells can be damaged by deprivation of blood oxygen (ischaemia) during stroke and other circulatory disturbances. David Attwell and colleagues show that ischaemic damage to oligodendrocytes causes elevation of intracellular Ca2+ levels through H+-dependent activation of TRPA1 receptors, and not via glutamate receptors of the NMDA type, as previously thought. The results provide a new mechanism and promising therapeutic targets for diseases as diverse and prevalent as cerebral palsy, spinal cord injury, stroke and multiple sclerosis.

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