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Related Experiment Videos

Peripheral nervous system pathology in relapsing experimental allergic encephalomyelitis.

R E Madrid, H M Wiśniewski

    Journal of Neurocytology
    |June 1, 1978
    PubMed
    Summary

    Experimental allergic encephalomyelitis in guinea pigs causes recurrent demyelination in nerve roots and ganglia. This study identifies damage at the nodes of Ranvier and discusses potential antigenic causes.

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    Area of Science:

    • Neuroscience
    • Immunology
    • Pathology

    Background:

    • Experimental allergic encephalomyelitis (EAE) is a model for demyelinating diseases.
    • Strain 13 guinea pigs develop relapsing EAE.
    • Primary demyelination in the peripheral nervous system is not fully understood.

    Purpose of the Study:

    • To investigate the pattern and nature of demyelination in peripheral nerves during relapsing EAE.
    • To examine the role of Schwann cells and the nodes of Ranvier in EAE pathogenesis.
    • To explore potential factors contributing to the selective vulnerability of anterior roots.

    Main Methods:

    • Induction of relapsing EAE in strain 13 guinea pigs.
    • Single nerve fiber analysis to study myelin and Schwann cell morphology.

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  • Histopathological examination of nerve roots and dorsal root ganglia.

    • Main Results:

    • Recurrent demyelination was observed in anterior roots and dorsal root ganglia.
    • Myelin destruction predominantly occurred at the nodal and paranodal regions.
    • Damage to the Schwann cell-axolemmal junction and formation of aberrant Schwann cell processes were noted.
    • Selective involvement of anterior roots was identified.

    Conclusions:

    • The findings suggest a specific pattern of demyelination in EAE affecting peripheral nerves.
    • Schwann cell abnormalities contribute to the pathology at the nodes of Ranvier.
    • Antigenic variations may influence the susceptibility of specific nerve structures like anterior roots.