Abstract
It has been shown, by a histological method of assessment, that exogenous triiodothyronine in doses from 5.0–500 ng per 100 g body weight significantly increases the rate of elongation of axons distal to a crush lesion of the sciatic nerve of the rat. The magnitude of the effect increases with dosage of the hormone, and the mean distance regenerated in 11 days is more than trebled in rats receiving the highest dosage tested. It appears likely that this effect is mediated through an increased rate of neuronal protein synthesis, but the present results do not exclude the possibility that axonal elongation is accelerated by other mechanisms. Further investigations of the mode of action of triiodothyronine, and of the functional specificity of the more rapidly regenerated axons, are required before any possible clinical application of the findings can be entertained.
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