Although the function of juxtaparanodal Kv1 channels in normal myelinated nerve fibers is not well understood, several lines of evidence suggest that disruption or loss of the myelin sheath can dramatically alter the conduction proper ties of an axon and reduce excitability. In some instances, this disruption appears to be almost entirely a consequence of aberrant localization and expression of Kv1 channels, as the use of Kv1 channel blockers can restore conduction (Bostock etal., 1981; Targ and Kocsis, 1985, 1986; Rasband et al., 1998; Nashmi et al., 2000). The consequences of demyelination and or myelin disruption for the localization and expression of Kv1 channels has been investigated mainly in two separate kinds of model systems: (1) experimentally demyelinated axons and (2) dysmyelinating, hypomyelinating, or demyelinating mutant mice. The evidence that Kv1 channels are important contributors to axonal dysfunction in each of these experimental paradigms is described next.
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