Experimental Model of Pyridoxine (B6) Deficiency-Induced Neuropathy

Abstract

A pyridoxine (B6) dietary deficiency was studied in female adult Sprague-Dawley rats by hind-limb walking-track analysis. Serum levels of pyridoxine and three metabolites were quantified by high-pressure liquid chromatography with fluorescence measurement. Morphometric analysis of the sciatic and posterior tibial nerves (from within the tarsal tunnel) was performed after 1 year on a diet deficient in vitamin B6. The B6-deficient rats developed abnormal walking-track patterns by 8 months, and these track parameters were different from age- and sex-matched normal diet control rats at the p < 0.05 level. Adding B6 at 10 parts per million to the diet then partially corrected these parameters, whereas the addition of 30 parts per million B6 corrected the abnormal pattern completely. Serum pyridoxal concentration correlated with the functional parameters, dropping from a mean of 115 mg per liter to 39.5 mg per liter (p < 0.05), and correcting with the B6 additive. Morphometric analysis demonstrated that the B6-deficient nerve from the tarsal tunnel had a decreased nerve fiber density (p < 0.001), with a normal total myelinated nerve fiber number, and an increased axon-to-myelin ratio (p < 0.003). It is concluded that a diet totally deficient in vitamin B6 results in a peripheral neuropathy.

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

“…Rats receiving a diet deficient in pyridoxine for one year developed abnormal walking-track patterns, however, when these rats received pyridoxine they partially recovered [301].…”

Interrelationships of undernutrition and neurotoxicity: Food for thought and research attention

“…Dietary deficiency of pyridoxine caused peripheral neuropathy in adult rats (Root and Longenecker, 1973; Dellon et al, 2001). Axonal abnormalities were associated with oligodendrocyte adaxonal ingrowths, a phenomenon common to beginning axonopathies in which the ensheathing cell sequesters and selectively removes effete and degenerate materials from the axon (Spencer and Thomas, 1974).…”

Evaluation Tools and Animal Models of Peripheral Neuropathies

“…A common hallmark of these neuropathies are the structural and functional alterations of the myelin sheath and axons in response to a metabolic dysfunction. Few animal models have been developed to study alcoholic or uraemic neuropathy [152][153][154][155] and neuropathy induced by pyridoxine or thiamine deficiency [156][157][158] . In accordance with their frequency and severity, diabetic neuropathies are the most studied diseases among all the PNS pathologies [for a general review, see 159 ].…”