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Pregnant and nursing Wistar rats were fed a thiamine-deficient diet, and their offspring were injected daily with pyrithiamine. The pathologic lesions in the suckling rats were examined at different times of development. There were distinct changes at 22 days of age, by which time the rats are weaned, and the morphogenesis of the cerebellum is almost completed. Before 22 days of age, there were no pathologic changes except for scattered petechial hemorrhages in the brain.

Following a single i.p. injection of 6-AN (10 mg/kg), the anterior horn cells of 20- and 25-month-old rats increased more in size and recovered slower from chromatolytic changes than those of 3-month-old rats. Neurofilamentous hyperplasia of the perikarya was more prominent in aged rats; proliferated neurofilaments were arranged in thick parallel bundles.

Lesions in the CNS induced by 6-aminonicotinamide (6-AN) presented a spongy state of the gray matter and neuronal chromatolysis. With aging of the experimental animals the lesions extended from the phylogenetically early developed structures to those developed later, i.e., from spinal gray matter, dentate nuclei, and brain stem nuclei through limbic structures and striatum to the cerebral cortex. Changes of the neurons were more prominent with aging.

Ultrastructure of neuronal chromatolysis and other lesions in the gray matter of the cervical cord due to 6-aminonicotinamide (6-AN) administration, an antinicotinamide, to rats, were followed up during a 35-days period. Neuronal chromatolysis which was prominent in the anterior horn cells in the acute stage, was completely recovered from via the temprary hyperchromasia of their cytoplasm. Their axons, however, which form the anterior nerve roots, did not show any particular changes throughout the whole period of the experiment. This evidence suggests that neuronal chromatolysis induced by 6-AN might not be the result of axonal damage, but was due to the direct action of 6-AN on the soma of the anterior horn cells.