Abstract

The vulnerability of immature rabbits to experimental allergic neuritis (EAN) was investigated. The incidence, severity and duration of EAN signs are described; histological changes occuring in dorsal roots and peroneal nervws were observed by light and electron microscopy. Unequivocal signs of EAN occured only in rabbits older than 4 weeks at the time of antigen challenge. Immature EAN rabbits differ in the course of the disease from adults in (a) lower incidence, (b) a greater recovery rate. The time of onset of signs and the duration of signs were not significantly different from the adult group. The results are interpreted in terms of the development of immunological competence, and relative rates of myelic synthesis and myelin degradation. As in the adult, EAN in immature rabbits is characteristically a segmental demyelinating, axon-sparing condition. Demyelination is largely mediated by cells of exogenous origin, though evidence for a contribution by circulating antibodies and degradation of myelin by the Schwann cell is discussed. The type of demyelination represented by EAN is contrasted with that occuring after diptheritic intoxication. The vulnerability of spinal roots to demyelination in EAN is interpreted in terms of the greater permeability of neural capillaries in roots compared with peripheral nerves. The functional significance of the splitting of myelin at the intraperiod line is considered to be related to the putative distribution of encephalitogenic basic protein. A hypothesis is proposed to account for the sparing of the Schwann cell plasma membrane in an autoimmune response which selectively degrades myelin.

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