Pyridoxine neuropathy: Correlation of functional tests and neuropathology in beagle dogs treated with large doses of vitamin B6

  title={Pyridoxine neuropathy: Correlation of functional tests and neuropathology in beagle dogs treated with large doses of vitamin B6},
  author={Ulrich Schaeppi and Georg J. Krinke},
  journal={Agents and Actions},
Neurologic examination, electrophysiologic testing and microscopic post-mortem examination was used to study the neuropathy induced in the beagle dog by administration of excessive amounts of vitamin B6.Two female dogs received repeated daily oral doses of 3 g. The treatment was ceased when the dogs developed severe general morbidity, including uncoordinated gait and abnormal neurologic symptoms. The symptoms were most severe during and early after cessation of treatment, and in general they… 

Neuropathological changes in dorsal root ganglia induced by pyridoxine in dogs

The results suggest that PDX-induced neuropathy is reversible in dogs; thus, dogs can be considered a good experimental model for research on neuropathy.

What can specific behavioural testing procedures contribute to the assessment of neurotoxicity in laboratory animals?

In case of relevant neurotoxicity subsequent specific behavioural tests might include the evaluation of complex neural functions such as integrated psycho-neuro-motor activity and memory that help to explain neurotoxicity and to assess behaviour at low levels of exposure.

High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.

It is demonstrated that high-dose pyridoxine administration can be used to produce a new mouse model for AN, and coffee or trigonelline as a main active compound of coffee extract can potentially facilitate recovery from pyrIDoxine-induced auditory neuropathy.

Vitamin B-6-Induced Neuropathy: Exploring the Mechanisms of Pyridoxine Toxicity

It is concluded that PDXK inhibition and consequently disrupted GABA neurotransmission is the most plausible mechanism of toxicity.

Alteration of neuronal cytoskeletal organization in dorsal root ganglia associated with pyridoxine neurotoxicity

The results indicate that an early morphological correlate of pyridoxine neurotoxicity is the accumulation of NF with MT-NF dissociation in the unipolar process of the DRG in the absence of extensive vacuolization, and that the observed cytoskeletal disruption may be related to an increased rate of NF protein synthesis together with mechanical obstruction of transport phenomena.

SP, CGRP changes in pyridoxine induced neuropathic dogs with nerve growth factor gene therapy

It is reasoned that NGF gene therapy in pyridoxine induced neuropathic dogs does not induce neuropathic pain with this dosage, even with increasing the expression of CGRP.

Differential vulnerability of 3 rapidly conducting somato-sensory pathways in the dog with vitamin B6 neuropathy

In anesthetized dogs with chronically implanted cortical electrodes somatic sensory-evoked potentials (SEPs) were produced by electrical stimulation at neural, muscular or cutaneous sites of the contralateral hind leg, which allows it to be concluded that in the dog afferents from the glabrous skin of the central pad conduct centrally via the dorsal columns, susceptible to vitamin B6 intoxication.

Neuropathic Pain models caused by damage to central or peripheral nervous system.



Pyridoxine megavitaminosis produces degeneration of peripheral sensory neurons (sensory neuronopathy) in the dog.

It is apparent that the peripheral neuropathy previously attributed to pyridoxine actually represents a toxic, peripheral sensory neuronopathy, and may reflect the selective permeability of blood vessels in the peripheral ganglia.

Clioquinol and 2,5-hexanedione induce different types of distal axonopathy in the dog

Light and electron microscope examination of central and peripheral nervous tissue from dogs intoxicated with 2,5-hexanedione revealed giant axonal swelling and distal axonal degeneration, by contrast, dogs receiving clioquinol showed a distalAxonopathy confined to the optic tract and the long spinal cord tracts, without any visible involvement of peripheral nerves.

Sensory and motor maximum nerve conduction velocity in the peripheral and central nervous system of the beagle dog

These testing procedures serve for quantitative assessment of possible impairment of impulse transmission in the central and peripheral sensory and motor pathway of beagle dogs used in routine toxicity studies.

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