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 - 1985/11
Y1 - 1985/11
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doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided alter the toxin was withdrawn.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doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided alter the toxin was withdrawn.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.
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U2 - 10.1212/wnl.35.11.1617
DO - 10.1212/wnl.35.11.1617
M3 - Article
C2 - 2997659
AN - SCOPUS:0022218535
SN - 0028-3878
VL - 35
SP - 1617
EP - 1622
JO - Neurology
JF - Neurology
IS - 11
ER -