Differential effect of chronic vitamin E deficiency on the development of neuroaxonal dystrophy in rat gracile/cuneate nuclei and prevertebral sympathetic ganglia.
Chronic vitamin E deficiency results in the premature and exaggerated development of neuroaxonal dystrophy (NAD) in primary sensory axon terminals in rat medullary gracile/cuneate nuclei, sites in which NAD develops normally with age. In the current study we determined if chronic Vitamin E deprivation had a similar effect on the development of NAD in the celiac/superior mesenteric sympathetic ganglia (C/SMG), another site with age-dependent NAD. The frequency of NAD failed to increase in the SMG of the same vitamin-E deficient animals in which a marked increase in severity of NAD was found in the gracile nucleus. These findings indicate that different populations of neurons are selectively involved in vitamin E deficiency and that the distribution of axonopathy in the E-deficient C/SMG does not duplicate the pattern of experimental diabetes and aging.
Schmidt
R E
RE
Department of Pathology (Division of Neuropathology), Washington University School of Medicine, St. Louis, MO 63110.
Coleman
B D
BD
Nelson
J S
JS
D000818:Animals; D001369:Axons / Q000648:ultrastructure*; D005728:Ganglia, Sympathetic / Q000473:pathology* / Q000648:ultrastructure; D008297:Male; D008526:Medulla Oblongata / Q000473:pathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D009474:Neurons / Q000473:pathology* / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D014810:Vitamin E / Q000032:analysis; D014811:Vitamin E Deficiency / Q000473:pathology* / Q000503:physiopathology
D014810:Vitamin E