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Damage to axons is mediated by the following: (1) failure in mitochondrial energy metabolism due to inhibition of the respiratory chain by nitric oxide, which in turn causes a decrease in Na + /K + ATPase activity and alters Na + ‐dependent glutamate transporters, (2) over‐expression of glutamate receptors, (3) oligodendroglial excitotoxicity, (4) massive influx of extracellular Ca ++ , (5) activation of proteases, and (6) impaired axonal transport