Abstract

The neurotoxicity induced by an excess of vitamin B6 in animals has been known for many years but the first human clinical cases have only recently been reported. All subjects showed paraesthesia and numbness as well as ataxia. The clinical examination showed a large sensory deficit with Achilles’ reflex loss. The electromyographic examination showed a large sensory wave amplitude decrease but no change in the motor conduction. Different rat models of pyridoxine-induced neuropathy exist. Here, we present results with a modified and improved intoxication schedule of an existing rat model. We describe in detail the evolution of the disease and show for the first time that 4-methylcatechol, an inducer of nerve growth factor (NGF) synthesis, improves the clinical status of the intoxicated animals and restores the morphological integrity of the large fibres. We conclude that (a) the pyridoxine-induced sensory neuropathy provides the pharmacologists with a valuable model for studying and evaluating new neurotrophic factors endowed with NGF-like properties and (b) this model can be included in the palette of experimental sensory neuropathies used in preclinical research for evaluating new putative neuroprotective drugs, the mechanisms of action of which are not known.

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