Alterations of nerve-muscle interaction during postnatal development influence motoneurone survival in rats.

The effect of temporary paralysis of rat soleus muscles shortly after birth on motoneurone survival was studied using retrograde labelling with HRP. Following a single application of alpha-bungarotoxin (alpha-BTX) at birth the muscles were paralysed for 24-48 h. The number of HRP-labelled motoneurones in the treated ventral horn of the spinal cord in 10-week-old rats decreased to 63.7% (+/- 2.7 S.E.M.) of the control ventral horn. This motoneurone loss occurs relatively late after alpha-BTX application, for in animals examined at 3-4 weeks of age, the number of labelled motoneurones in the treated ventral horn was not reduced. When paralysis of the soleus muscles was extended to 6-8 days by application of an additional alpha-BTX implant, then by 10 weeks of age only 34.7% (+/- 1.5 S.E.M.) of soleus motoneurones were present. Thus, prolonging the duration of paralysis reduced the number of surviving motoneurones. Furthermore, the mean area of motoneurones that survived alpha-BTX treatment was smaller than that of controls. There was also a shift in the size distribution of the motoneurones in that there was a relative increase in the proportion of small motoneurones. This finding is similar to observations on motoneurone sizes after neonatal nerve injury. Thus, interruption of neuromuscular interaction during early postnatal development causes many motoneurones to die, and in addition alters the size distribution of the remaining cells.