Abstract
Auditory evoked far-field potentials were recorded from mature quaking mice and their littermate controls. There was a significant prolongation in the latencies of all FFP peaks in the quaking mutants. Examination of the interaction between group (normal, quaking) and for selected pair-wise peak comparisons showed that the degree of retardation was not uniform for each FFP peak. In view of the reported histological and biochemical findings that the CNS of the quaking mutant is specifically deficient in myelin, we conclude that slowed conduction in the quaking mouse brain is due to myelin deficiency and that non-uniform retardation of each FFP peak reflects regional variation in the extent of myelin deficiency. These data suggest that the changes in interpeak latencies of far-field potentials may be useful in identifying the demyelinated region(s) of the diseased central nervous system.
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