Abstract
Histofluorescence microscopy revealed extensive damage to bulbospinal catecholamine and indolamine axons in rats with paralysis induced by experimental allergic encephalomyelitis. The damaged axons were almost invariably located near perivascular inflammatory foci. Increased fluorescence intensity observed in affected axons and in their nuclei of origin is consistent with a build-up of transmitter substance similar to that following axonal transection. These results caution against over-emphasizing demyelination as the pathogenetic basis of experimental allergic encephalomyelitis. Injury to central monoaminergic neurons may be an important determinant of the somatic and visceromotor manifestations of the disease.
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