Degeneration of peripheral nervous system in rats experimentally induced by methylmercury intoxication

Neurol Sci. 2013 May;34(5):663-9. doi: 10.1007/s10072-012-1100-3. Epub 2012 Apr 25.

Abstract

The objective of this study is to elucidate the primary action of methylmercury chloride (MMC) intoxication on peripheral nervous system. We chronologically observed the pathological changes of sciatic nerve, dorsal root ganglion (DRG) neurons, ventral and dorsal roots in rats given 4 mg/kg/day of MMC on consecutive days and killed on days 11, 15, 18 and 21. On day 11, an initial axonal degeneration of type B neuron occurred, predominantly in the distal portions of sciatic nerve. The DRG type A neuron was infiltrated by MRF-1-positive macrophages on day 11. Electron microscopy also demonstrated degenerated mitochondria in type A neuron. On day 21, most of type A neurons seemed to have disappeared. However, type B neurons were well preserved. Immunoblotting with monoclonal antibodies, P0 and neurofilament, demonstrated that both of proteins significantly decreases from day 15. In conclusion, these results indicate that the primary action on type A neuron is the neuron body that consequently results in an anterograde degeneration of nerve fibers, while the type B neuron degeneration occurs in a dying-back process in this subacute model. These findings suggest that the mechanisms involved in the degeneration induced by MMC vary and may depend on certain intrinsic factors peculiar to these neurons.

MeSH terms

  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Axons / pathology
  • Disease Models, Animal
  • Ganglia, Spinal / pathology*
  • Ganglia, Spinal / ultrastructure
  • In Situ Nick-End Labeling
  • Male
  • Mercury Poisoning, Nervous System / etiology*
  • Mercury Poisoning, Nervous System / pathology*
  • Methylmercury Compounds / toxicity*
  • Microscopy, Electron, Transmission
  • Myelin P0 Protein / metabolism
  • Myelin Sheath / metabolism
  • Myelin Sheath / pathology
  • Nerve Degeneration / chemically induced*
  • Nerve Degeneration / pathology
  • Nerve Tissue Proteins / metabolism
  • Neurons / pathology
  • Neurons / ultrastructure
  • Rats
  • Rats, Wistar
  • Sciatic Nerve / pathology*
  • Time Factors

Substances

  • Amyloid beta-Protein Precursor
  • Methylmercury Compounds
  • Myelin P0 Protein
  • Nerve Tissue Proteins