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Sodium channel blockers and axonal protection in neuroinflammatory disease.

Although demyelination is a cardinal feature of neuroinflammatory conditions such as Guillain–Barre syndrome (GBS) and multiple sclerosis, axonal degeneration also occurs in these disorders. Because loss of axons causes permanent, non-remitting loss of neurological function, there is substantial interest in protection of axons in these situations. Protection of axons within white matter and peripheral nerves, however, is likely to require strategies different from those that might be expected to be protective in grey matter of the nervous system; the higher surface-to-volume ratio and different complement of molecules that are expressed in axons compared with neuronal cell bodies imply that the molecular mechanisms underlying axonal degeneration are different from those that cause neurons to die. Studies over the past decade have demonstrated that a sustained sodium influx through voltage-gated sodium channels can trigger reverse sodium–calcium exchange which imports damaging levels of calcium into axons after they are exposed to insults such as anoxia, thereby activating injurious calcium-mediated processes (Stys et al ., 1992 a ). Persistent sodium currents have, in fact, been demonstrated along the trunks of axons within the CNS (Stys et al ., 1993) and PNS (Tokuno et al ., 2003), and sodium channel blockers have been shown to have a protective effect, preventing axonal degeneration when axons are exposed to anoxia (Stys et al ., 1992 b ). A link to …