Transient disruption of nerve-muscle interaction shortly after birth permanently alters the development of the rat soleus muscle.

Transient paralysis of the rat soleus muscle shortly after birth leads to a permanent loss of motoneurones as revealed by retrograde labelling. Here we show that this loss of motoneurones is reflected in a reduction in the number of motor units. Soleus muscles in normal adult rats were found to have 27 (+/-0.6 S.E.M., n = 9) motor units. However, in muscles which had been treated with alpha-bungarotoxin (BTX) at birth and 3 days of age, causing paralysis lasting for 6-8 days, only 15(+/-0.6 S.E.M., n = 5) motor units remain. The effects of paralysis on the ability of the adult soleus muscle to develop force was also tested. Following treatment with a single BTX implant at birth, causing paralysis for 2-3 days, soleus muscles develop less tension (73.7% +/- 4.5 S.E.M., n = 8) and weigh less (88.2% +/- 3.8 S.E.M., n = 13) than their unoperated controls. This loss of muscle force is caused by a loss of muscle fibres, which in muscles that had been paralysed at birth was 81.4% (+/-4.1 S.E.M., n = 5) of control. Prolonging the duration of paralysis led to a greater reduction in force production, weight and the number of muscle fibres. Those muscles which had been paralysed at birth also took longer to relax during single twitch contractions. In addition, whereas normal soleus muscles contain around 20% of muscle fibres that do not react with antibodies to slow myosin HC, in soleus muscles paralysed at birth, 100% of the fibres reacted with this antibody. This study shows that disruption of neuromuscular interaction for a brief period after birth leads to a loss of motoneurones and a permanent impairment of muscle function.