Springer Online Journal Archives 1860-2000
Summary Developmental changes in the cerebellum of neonatal Long-Evans rats with lead encephalopathy were studied by Golgi technique and by light and electron microscopy. Lead encephalopathy was produced by administering daily doses of lead acetate (600 mg of lead acetate/kg of body weight) through an esophageal catheter. Histopathologic changes were observed at 3, 5, 8, 10, 13, and 15 days of age. Matrix cells and neuroblasts of the external granular layer were minimally altered prior to day 8 but thereafter the number of mitotic figures per folium decreased moderately and the number of pyknotic cells increased markedly. The thickness of the molecular layer in lead poisoned animals persistently lagged behind that of control animals after 3 days. Purkinje cells survived the cerebellar alterations of lead encephalopathy very well for the first 5–8 days. However, the rate of Purkinje cell maturation dropped off and at 10 days many still possessed the “mitre” of reticular cytoplasm and the perisomatic processes that are so characteristic of 5–8-day old Purkinje cells. This was particularly true for Purkinje cells located superficial to the “edematous cavities” produced by lead intoxication. The perisomatic processes of these Purkinje cells maintained synaptic contact with climbing fibers, whereas the climbing fibers of control animals had formed asymmetric synapses in the lower dendritic field and the cell soma had symmetric basket fiber synapses. A great variation existed in dendritic growth. Morphologically the neurons were minimally altered by lead intoxication until late in the disease process. The observed neuronal damage supports the suggestion that it is secondary to vascular disruption.
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