Windebank A J, Low P A, Blexrud M D, Schmelzer J D, Schaumburg H H
Neurology. 1985 Nov;35(11):1617-22. doi: 10.1212/wnl.35.11.1617.
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doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided after the toxin was withdrawn.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.
当大鼠接受大剂量的吡哆醇（剂量大到足以在人类中引起神经病变）时，这些动物会出现步态共济失调，在毒素撤出后症状会消退。通过使用定量组织学技术，我们发现感觉系统纤维出现轴突变性，而来自腹根的纤维未受影响。尽管变性接近背根神经节，但神经节中的神经元并未变性。我们发现神经的氧消耗没有早期减少，这表明氧化代谢受损不是主要事件。
