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Lead encephalopathy was induced in developing Long-Evans rats by adding lead carbonate (4% w/w) to the diet of nursing mothers immediately after delivery. The suckling rats avidly accumulated lead, and by the 30th postnatal day the concentration of lead in the young-rat brain was nearly four times that in the mother. The overall effect of lead intoxication was retardation of growth of neural tissues without reduction of cell populations. The formation of myelin was altered and its cerebral content significantly reduced. Axons were reduced in size, and the number of myelin lamellae in the sheaths was also reduced. However, the relationship between axon diameter and myelin lamellae was preserved. Results of biochemical studies of the composition of the brain lipids were indistinguishable in lead-exposed and control animals. These biochemical studies included analyses of the neural constitution of phospholipids and gangliosides, the composition of the major gangliosides of the myelin subfraction, and the fatty acid composition of cerebrosides, sulfatides, and ceramides purified from brain. The effect of lead intoxication in the developing rat is one of hypomyelination. The hypomyelination appears to be primarily related to retarded growth and maturation of the neuron and not a reflection of a defect in the myelinating glia or a delay in the initiation of myelination.
Krigman et al. (1974) studied this question.