EXPERIMENTAL allergic encephalomyelitis (EAE) and experimental allergic neuritis (EAN) are autoimmune demyelinating conditions brought about by sensitisation to central and peripheral myelin extracts, respectively. The lesions are the result of a delayed hypersensitivity-type reaction which can be passively transferred by lymphoid cells but not by sera1–4. Demyelination occurs in areas of cellular infiltrate. This process is mediated in part by mononuclear cells which invade and phagocytise the target myelin tissue. A vesicular transformation of myelin sheaths is known to occur in close proximity to these invading mononuclear cells5–7. The nature of the myelin vesiculation is unclear; however, these changes have been emphasised as a characteristic accompaniment of autoimmune demyelination in experimental animals and in human peripheral nerve disease8. The present study reports the occurrence of the same type of myelin alteration in excised rat peripheral nerve fibres when incubated under conditions which promote a selective influx of calcium ions into the tissues.
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SCHLAEPFER, W. Vesicular disruption of myelin simulated by exposure of nerve to calcium ionophore. Nature 265, 734–736 (1977). https://doi.org/10.1038/265734a0
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