Neonatal paralysis of the rat soleus muscle selectively affects motoneurones from more caudal segments of the spinal cord

Abstract

Transient paralysis of the rat soleus muscle shortly after birth leads to permanent muscle weakness, loss of muscle fibres and the death of motoneurones. The soleus muscle receives its innervation from motoneurones whose axons exit the spinal cord either via the L4 ventral ramus or in the more caudal part of the cord via the L5 ventral ramus. Whether both populations of motoneurones are equally affected by neonatal paralysis was studied here. In soleus muscles paralysed with α-bungarotoxin shortly after birth and examined 8–10 weeks later, there is no loss of force or muscle fibres in the part of the muscle supplied by axons in the L4 ventral ramus. Loss of force and muscle fibre numbers occurs only in the part of the muscle supplied by axons in the L5 ventral ramus. In a normal adult soleus 30.3 ± 2.4% of muscle force is produced by stimulating the L4 ventral ramus and 69.0 ± 5.5% by stimulating the L5 ventral ramus. In soleus muscles treated with α-bungarotoxin 28 ± 1.4% of the force produced by the contralateral control soleus was generated by axons in the L4 ventral ramus and only 20.3 ± 5.6% by stimulating the L5 spinal nerve. The number of muscle fibres supplied by either ventral ramus in control and experimental muscles confirmed that the decrease of force after treatment with α-bungarotoxin can be accounted for by loss of muscle fibres supplied by axons in the L5 ventral ramus. The reduced force production and muscle fibre numbers was due to a selective loss of motoneurones that had their axons in the L5 ventral ramus. The number of axons to soleus in the L4 ventral ramus was 9.3 ± 0.7 in controls and 10.3 ± 0.9 in the experimental animals, whereas the L5 ventral ramus contained 17.2 ± 0.7 in controls and only 4.7 ± 1.7 in the experimental animals. Thus paralysis of the soleus muscle at birth selectively affects motoneurones in the more caudal part of the spinal cord, suggesting that the more cranial motoneurones are more mature and less likely to be influenced by lack of neuromuscular interaction at the time of birth.