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Testosterone fails to rescue motoneurons from axotomy-induced death in young rats
1Department of Cell Biology and Anatomical Sciences, City University of New York Medical School, NY 10031.
Abstract:
This study was undertaken to determine whether testosterone acting on muscle alone could enhance motoneuron survival after axotomy. Facial nerves were transected unilaterally in 10-day old rats in which androgen receptors were already present in skeletal muscle but not yet developed in motoneurons. Testosterone treatment lessened chromatolysis but failed to reduce neuronal loss which reached more than 50% 2 weeks postaxotomy. The inefficacy of testosterone was attributed to the death of motoneurons before they could re-establish synaptic contact with targets, thereby rendering target-derived trophic substances stimulated by testosterone unable to rescue motoneurons in a timely manner. The present finding is consistent with our hypothesis that functional neuromuscular connectivity is a prerequisite for testosterone to promote neuronal survival.
Insights
Testosterone did not improve motoneuron survival after nerve injury in young rats. Functional neuromuscular connections are necessary for testosterone to aid neuronal survival and recovery.
Area of Science:
- Neuroscience
- Endocrinology
- Muscle physiology
Background:
- Testosterone influences neuronal function, but its direct effect on motoneuron survival post-axotomy is unclear.
- Androgen receptors are present in skeletal muscle before motoneuron development in neonatal rats.
Purpose of the Study:
- To investigate if testosterone, acting solely on skeletal muscle, can enhance motoneuron survival after facial nerve axotomy.
- To determine the necessity of functional neuromuscular connectivity for testosterone's neuroprotective effects.
Main Methods:
- Unilateral facial nerve transection in 10-day-old rats.
- Testosterone administration to assess effects on motoneuron survival and chromatolysis.
- Evaluation of neuronal loss and synaptic re-establishment.
Main Results:
- Testosterone treatment reduced chromatolysis but did not prevent over 50% motoneuron loss 2 weeks post-axotomy.
- Motoneuron death occurred before synaptic contact re-establishment.
- Testosterone's efficacy was limited by the lack of timely target-derived trophic support.
Conclusions:
- Testosterone alone, without established functional neuromuscular connectivity, is insufficient to promote motoneuron survival after axotomy.
- Functional neuromuscular connectivity is a prerequisite for testosterone to exert a neuroprotective effect on motoneurons.
- Target-derived trophic factors, stimulated by testosterone, require timely synaptic contact to rescue axotomized motoneurons.