Abstract
BackgroundPyridoxine (PDX; vitamin B6), is an essential vitamin. PDX deficiency induces various symptoms, and when PDX is misused it acts as a neurotoxicant, inducing severe sensory neuropathy.ResultsTo assess the possibility of creating a reversible sensory neuropathy model using dogs, 150 mg/kg of PDX was injected subcutaneously into dogs for 7 days and body weight measurements, postural reaction assessments, and electrophysiological recordings were obtained. In addition, the morphology of dorsal root ganglia (DRG) and changes in glial fibrillary acidic protein (GFAP) immunoreactive satellite glial cells and ionized calcium-binding adapter molecule 1 (Iba-1) immunoreactive microglia/macrophages were assessed at 1 day, 1 week, and 4 weeks after the last PDX treatment. During the administration period, body weight and proprioceptive losses occurred. One day after the last PDX treatment, electrophysiological recordings showed the absence of the H-reflex in the treated dogs. These phenomena persisted over the four post-treatment weeks, with the exception of body weight which recovered to the pre-treatment level. Staining (CV and HE) results revealed significant losses of large-sized neurons in the DRG at 1 day and 1 week after PDX treatment cessation, but the losses were recovered at 4 weeks post-treatment. The Iba-1 and GFAP immunohistochemistry results showed pronounced increases in reactive microglia/macrophage and satellite glial cell at 1 day and 1 week, respectively, after the last PDX treatment, and thereafter, immunoreactivity decreased with increasing time after PDX treatment.ConclusionsThe results suggest that PDX-induced neuropathy is reversible in dogs; thus, dogs can be considered a good experimental model for research on neuropathy.
Highlights
Pyridoxine (PDX; vitamin B6), is an essential vitamin
Body weight measurements Weight loss was observed in the PDX-treated group (Fig. 1) with a significant relative decrease from the body weight before PDX treatment (100% ± 0%) to that after the last PDX treatment (87.3% ± 3.8%) (P < 0.0001)
There was no significant difference in the relative body weight before PDX treatment (100 ± 0%) and that at 4 weeks after the last PDX treatment (97.9% ± 4.8%) (P = 0.6579)
Summary
Pyridoxine (PDX; vitamin B6), is an essential vitamin. PDX deficiency induces various symptoms, and when PDX is misused it acts as a neurotoxicant, inducing severe sensory neuropathy. Pyridoxine (PDX), along with pyridoxal and pyridoxamine, are compounds that can be referred to as vitamin B6. PDX is considered an essential vitamin, and a PDX deficiency induces various symptoms [1]. There are many disorders that involve invasion of peripheral nerves, inducing sensory neuropathy, which is caused by genetic diseases, metabolic imbalance, endocrine disease, toxins, fluoroquinolone toxicity, inflammation, and physical trauma. Many clinical trials have been conducted to develop a treatment for sensory neuropathy; it is apparent that more animal models of sensory neuropathy are required. Dogs are considered valuable animal models because they are more similar to humans than rodents. Fewer neurological studies have been conducted using canine models than rodent models [7]
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