Pyridoxine neuropathy in rats: Specific degeneration of sensory axons

Anthony J. Windebank, Phillip A. Low, Marceil D. Blexrud, James D. Schmelzer, Herbert H. Schaumburg

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided alter the toxin was withdrawn.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.

Original languageEnglish (US)
Pages (from-to)1617-1622
Number of pages6
JournalNeurology
Volume35
Issue number11
StatePublished - 1985

Fingerprint

Gait Ataxia
Histological Techniques
Pyridoxine
Spinal Nerve Roots
Spinal Ganglia
Oxygen Consumption
Ganglia
Axons
Neurons
Degeneration
Fiber
Rat

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Windebank, A. J., Low, P. A., Blexrud, M. D., Schmelzer, J. D., & Schaumburg, H. H. (1985). Pyridoxine neuropathy in rats: Specific degeneration of sensory axons. Neurology, 35(11), 1617-1622.

Pyridoxine neuropathy in rats : Specific degeneration of sensory axons. / Windebank, Anthony J.; Low, Phillip A.; Blexrud, Marceil D.; Schmelzer, James D.; Schaumburg, Herbert H.

In: Neurology, Vol. 35, No. 11, 1985, p. 1617-1622.

Research output: Contribution to journalArticle

Windebank, AJ, Low, PA, Blexrud, MD, Schmelzer, JD & Schaumburg, HH 1985, 'Pyridoxine neuropathy in rats: Specific degeneration of sensory axons', Neurology, vol. 35, no. 11, pp. 1617-1622.
Windebank AJ, Low PA, Blexrud MD, Schmelzer JD, Schaumburg HH. Pyridoxine neuropathy in rats: Specific degeneration of sensory axons. Neurology. 1985;35(11):1617-1622.
Windebank, Anthony J. ; Low, Phillip A. ; Blexrud, Marceil D. ; Schmelzer, James D. ; Schaumburg, Herbert H. / Pyridoxine neuropathy in rats : Specific degeneration of sensory axons. In: Neurology. 1985 ; Vol. 35, No. 11. pp. 1617-1622.
@article{8160a65c8ceb40fcb7e6ca6775258f16,
title = "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 alter 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.",
author = "Windebank, {Anthony J.} and Low, {Phillip A.} and Blexrud, {Marceil D.} and Schmelzer, {James D.} and Schaumburg, {Herbert H.}",
year = "1985",
language = "English (US)",
volume = "35",
pages = "1617--1622",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "11",

}

TY - JOUR

T1 - Pyridoxine neuropathy in rats

T2 - Specific degeneration of sensory axons

AU - Windebank, Anthony J.

AU - Low, Phillip A.

AU - Blexrud, Marceil D.

AU - Schmelzer, James D.

AU - Schaumburg, Herbert H.

PY - 1985

Y1 - 1985

N2 - When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided alter 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.

AB - When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided alter 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.

UR - http://www.scopus.com/inward/record.url?scp=0022218535&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022218535&partnerID=8YFLogxK

M3 - Article

C2 - 2997659

AN - SCOPUS:0022218535

VL - 35

SP - 1617

EP - 1622

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 11

ER -