Peripheral nerve crush during the early neonatal period results in the death of a large proportion of affected motoneurons and abnormal dendritic development in those which survive. The present study reports the effects of neonatal dorsal root section on motoneurons supplying the extensor digitorum longus muscle of the rat. This lesion did not result in motoneuron death, but did disrupt subsequent dendritic development. In cells retrogradely labelled with cholera toxin subunit B conjugated to horseradish peroxidase, there was little change in adult dendritic morphology in the transverse plane, where abnormalities associated with loss of efferent contact and cell death have been found. However, there was a caudal expansion of the dendritic field, an effect seen following nerve crush but not after blockade of neuromuscular transmission alone. The results show that disruption of dorsal root sensory inputs alone can affect the dendritic development of motoneurons but does not cause their death. In conjunction with our earlier findings, it is clear that both afferent and efferent connections are required for normal dendritic development, and disruption of either has a characteristic effect on survival and dendritic morphology.