Levocarnitine acetyl promotes the regeneration of peripheral sensory axons and reduces the hypertrophy of axotomized spinal cord motoneurons in rats

Abstract In previous studies, the neurotrophic action of levocarnitine acetyl on the regeneration of the sciatic nerve in rats has been demonstrated. The present study investigated the particular effect of levocarnitine acetyl on the initial stages of sciatic nerve regeneration. In the first 8 days after sciatic nerve lesion caused by crushing (Group A) or cutting (Group B), the rats of both groups were divided into 2 subgroups: treated rats received daily intraperitoneal levocarnitine acetyl (a megadose of 100mg in saline solution); untreated rats only received saline solution. Treatment started on the day of operation. The regeneration growth rate of sensory fibres was studied using the pinch test. The size of the axotomized spinal motoneurons was studied using retrograde axonal tracers (horseradish peroxidase or Fast blue). The results showed that: (a) levocarnitine acetyl promoted the elongation of sensory fibres in the first 8 days following the crushing or sectioning of the sciatic nerve, but the data were only statistically significant (p < 0.01) for the first 3 days after crushing; (b) levocarnitine acetyl accelerated the velocity of sensory fibre regeneration when compared to untreated rats by 16% in the first 3 days after nerve crushing, by 14% in the first 4 days after nerve section, and by 32% from the 5th to the 8th day after nerve section; (c) levocarnitine acetyl promoted a significant reduction in spinal motoneuron hypertrophy when compared to untreated rats at both 4 and 8 days after sciatic nerve section. The composite results seem to indicate that levocarnitine acetyl antagonizes the metabolic shock of axotomized neurons and also promotes repair, synthesis and transport of organic material and reorganization of the cytoskeleton in the regenerated axon.