Neonatal nerve injury causes long-term changes in growth and distribution of motoneuron dendrites in the rat.

Disruption of neuromuscular contact by nerve-crush during the early postnatal period results in the death of a large proportion of affected motoneurons. Increased activity and abnormal reflex responses are evident in those that survive. We have studied the aberrant dendritic morphology of surviving cells and have attempted to correlate the observed alterations in morphology with the above experimental findings. Motoneurons supplying the extensor hallucis longus muscles of the rat were retrogradely labelled with cholera toxin subunit-B conjugated to horseradish peroxidase. The dendritic tree of labelled cells was analysed in adult animals having undergone unilateral sciatic nerve-crush at birth. Unoperated control animals were also examined. Following nerve-crush at birth, total visible dendritic length was more than 30% smaller than control cells in the transverse plane. This decrease was confined largely to the medially directed segments of the dendritic field and appeared to be due to a reduction in dendritic branching combined with a failure to achieve the correct branch length. There was no overall change in total visible dendritic length in the longitudinal plane, but a reorientation of dendrites in favour of rostrodorsal regions was observed. There was no alteration in dendritic length in cells contralateral to the nerve injury. These results show that nerve injury during early postnatal development produces lasting changes in the distribution of motoneuron dendrites. The localized nature of these changes may explain the altered activity and induced death of motoneurons seen after neonatal nerve-crush.