Hexacarbon neuropathy: cell body changes are early, dynamic, and specific.
To study the evolution of cell body alterations during toxic neuropathy we exposed rats to the prototype neurotoxin 2,5-hexanedione and examined perikarya of lumbar dorsal root ganglia with electron microscopy and stereology at three stages of neuropathy. Compared to unintoxicated controls, neurons from rats with incipient (four weeks) and intermediate (six to seven weeks) neuropathy showed dispersion of Nissl substance and significant decreases (p less than 0.001) in the volume fractions of Nissl bodies, but not of mitochondria or Golgi apparatus. However, at advanced (twelve to fourteen weeks) stages the volume fraction of Nissl bodies had increased and no longer differed from that of controls; distinct chromatolysis-like changes also became prominent. To evaluate the specificity of this remodeling we compared current morphometric results to data from rats exposed to acrylamide monomer and found significant differences (p less than 0.001) in the volume fractions of Nissl bodies and mitochondria. We conclude: (1) in axonopathy, cell body remodeling occurs early and advances as a dynamic, evolving process, and (2) distinct differences in the patterns of cell body changes can distinguish the neuropathies studied, implying distinct cell body functions.[1]References
- Hexacarbon neuropathy: cell body changes are early, dynamic, and specific. Sterman, A.B. Ann. Neurol. (1984) [Pubmed]
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