SCHWANN CELL RESPONSES DURING RECURRENT DEMYELINATION AND THEIR RELEVANCE TO ONION‐BULB FORMATION
Cedric S. Raine
Abstract
Cedric S. Raine
Abstract
Raine C.S. (1977) Neuropathology and Applied Neurobiology 3, 453–470 Schwann cell responses during recurrent demyelination and their relevance to onion‐bulb formation Morphological findings from the spinal nerve roots of six rabbits afflicted with chronic, relapsing EAE are presented. The fate of the Schwann cell subsequent to demyelination has been followed. It has been found that the original Schwann cell does not effect remyelination and that pockets of its cytoplasm are displaced by a new remyelinating cell. These pockets assume positions lateral to the main fibre, sometimes invested by cytoplasm from a separate, apparently healthy Schwann cell. At times during remyelination, difficulty was encountered in determining which profiles were axonal and which were Schwannian. However, plasmalemmal specialisations peculiar to Schwann cells, some of them described here for the first time, permitted positive identication in most cases. After several episodes of demyelination, each followed by rapid remyelination, supernumerary Schwann cells were common but, over the 24‐month period of study, profiles consistent only with primitive onion‐bulb formations were found. It is concluded that advanced (typical) onion‐bulb formation is not a feature of repeated demyelination per se but rather belongs to the hereditary, metabolic defects of the PNS, conditions in which the Schwann cell might be rendered impotent to form myelin.
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Raine C.S. (1977) Neuropathology and Applied Neurobiology 3, 453–470 Schwann cell responses during recurrent demyelination and their relevance to onion‐bulb formation Morphological findings from the spinal nerve roots of six rabbits afflicted with chronic, relapsing EAE are presented. The fate of the Schwann cell subsequent to demyelination has been followed. It has been found that the original Schwann cell does not effect remyelination and that pockets of its cytoplasm are displaced by a new remyelinating cell. These pockets assume positions lateral to the main fibre, sometimes invested by cytoplasm from a separate, apparently healthy Schwann cell. At times during remyelination, difficulty was encountered in determining which profiles were axonal and which were Schwannian. However, plasmalemmal specialisations peculiar to Schwann cells, some of them described here for the first time, permitted positive identication in most cases. After several episodes of demyelination, each followed by rapid remyelination, supernumerary Schwann cells were common but, over the 24‐month period of study, profiles consistent only with primitive onion‐bulb formations were found. It is concluded that advanced (typical) onion‐bulb formation is not a feature of repeated demyelination per se but rather belongs to the hereditary, metabolic defects of the PNS, conditions in which the Schwann cell might be rendered impotent to form myelin.
Key concepts: Remyelination, Schwann cell, Myelin, Biology, Cytoplasm, Neuroscience, Anatomy, Pathology