Purpose: We have previously demonstrated that systemic administration of testosterone propionate (TP) can accelerate the functional recovery from hind limb paralysis following sciatic nerve injury in the rat. In this study, we looked at the molecular mechanisms underlying this phenomenon. Methods: Castrated adult male rats received a right side sciatic nerve crush at the level of the sciatic notch, with the left side serving as control. Half the animals received a subcutaneous implant of TP, the others were sham implanted. Animals were sacrificed at 1, 3, 7 and 10 days post-operative. Lumbar spinal cord tissue was harvested and in situ hybridization was performed using a cytoskeletal cDNA probe complementary to βII-tubulin. Results: On the injured side, sciatic motoneuron tubulin mRNA levels were increased in all groups at all time points. At 3 and 7 days postop, the TP treated group had significantly higher levels of tubulin mRNA. Conclusions: These results suggest that testosterone enhances the rate of regeneration by increasing the neuronal cytoskeletal response after axonal injury. Further, these results, coupled with the results from previous experiments in other rodent models, suggest a common mechanism for gonadal steroid action on regenerating motoneurons across species.
|Original language||English (US)|
|Number of pages||8|
|Journal||Restorative Neurology and Neuroscience|
|State||Published - Dec 1 2001|
ASJC Scopus subject areas
- Developmental Neuroscience
- Clinical Neurology