Myelin development and nutritional insufficiency.

Abstract

Postnatal undernourishment does not greatly retard the generation of rat brain cells, although there is a slight reduction in total cell numbers and brain size. Possibly the maturation of cells is more severely affected. The ratio of myelinated to non-myelinated fibers is greatly reduced in the corpus callosum and pyramidal tract, and presumably in other areas as well. There is only a slight reduction in the numbers of myelin lamellae for axons of a given size. The recovery of brain myelin and the incorporation of radioactive precursors into purified myelin proteins and lipids are all greatly reduced, leading to a comparatively severe reduction in the brain myelin concentration. The myelin composition is only slightly altered, possibly as a result of delay in its normal chemical maturation. The actual vulnerable period that produces a lasting myelin deficit is the early period that includes oligodendroglia cell proliferation, whereas undernutrition restricted to a later period that includes the actual peak of myelin does not cause a lasting reduction in the brain myelin concentration. The belief that stunting the postnatal proliferation of oligodendroglia largely accounts for the myelin effect has not been substantiated by direct analysis of cell numbers. Consequently, the observed hypomyelination likely results from a failure of oligodendroglia to mature and to initiate myelin formation. The myelin deficit appears largely uniform throughout the brain. Indirect evidence in human studies indicate that comparable effects appear in undernourished infants.