Abstract
Osmic acid preparations of sciatic nerves and brachial plexuses of animals receiving a diet deficient in vitamin B but containing an adequate amount of vitamin G evidenced blackened material of the same type, amount, and distribution as was observed in control animals receiving adequate amounts of B and G. Nerves stained by the sudan III method at no time showed evidence of degenerative changes in either group. In the central nervous system, disseminated foci of hemorrhage or intense congestion of one or both sides involved the nuc. of Deiters, the chief vestibular nuc, the nuc. of Bechterew, and the nuc. solitarius in 75% of the animals in the deficient group. Cellular damage appeared to vary with the time left on experiment after the development of symptoms, and was observed most consistently in the regions of the nuc. of Deiters, the nuc. of Bechterew, the chief vestibular nuc, and the nuc. solitarius. These data indicate that the site of the lesion responsible for the symptomatology as-sociated with the lack of vitamin B in the rat is in the central rather than in the peripheral nervous system.