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Pyridoxine neuropathy in rats: specific degeneration of sensory axons.

Abstract
When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided after the toxin was withdrawn. By using quantitative histologic techniques, we found axonal degeneration of sensory system fibers and that the fibers derived from the ventral root were spared. Although the degeneration approached the dorsal root ganglion, neurons in the ganglion did not degenerate. We found no early decrease in oxygen consumption of nerve, suggesting that impaired oxidative metabolism was not the primary event.
AuthorsA J Windebank, P A Low, M D Blexrud, J D Schmelzer, H H Schaumburg
JournalNeurology (Neurology) Vol. 35 Issue 11 Pg. 1617-22 (Nov 1985) ISSN: 0028-3878 [Print] United States
PMID2997659 (Publication Type: Journal Article)
Chemical References
  • Pyridoxine
Topics
  • Animals
  • Axons (pathology, physiopathology)
  • Male
  • Neural Conduction
  • Oxygen Consumption
  • Peripheral Nervous System Diseases (chemically induced, pathology, physiopathology)
  • Pyridoxine (adverse effects)
  • Rats
  • Rats, Inbred Strains

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