MYELINATION OF THE OVINE CNS WITH SPECIAL REFERENCE TO BORDER DISEASE. II. QUANTITATIVE ASPECTS*

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Abstract
Myelination of the ovine CNS with special reference to Border disease. II. Quantitative aspectsSemithin Araldite sections and electron micrographs of the dorsal funiculus of spinal cord of sheep fetuses have been examined by methods devised to quantitate certain aspects of myelination. The data relating to axon size and shape, numbers of myelin lamellae, numbers and types of glial cells in normal fetuses have been compared with similar data obtained from an age‐matched series of fetuses affected with Border disease (BD). It was found that the enlargement of axons normally associated with the initial phases of myelination was greater in affected fetuses and, together with the accompanying irregularities of profile, tended to persist throughout gestation. In BD fetuses the rate and degree of myelination was reduced and the high periodicity which characterizes early myelin persisted into late gestation. Mature oligodendrocytes in BD fetuses were reduced by up to 40%, the normal total complement of glial cells being made up by cells with the morphology of multipotential (Type III) glial cells. It is tentatively concluded that Border disease affects the differentiation of oligodendrocytes from their precursors and thus leads to reduced myelin formation. Border disease is compared with relevant experimental and natural conditions and some similarities with Quaking in the mouse are indicated.