It has previously been shown that motoneurones die when neuromuscular interaction is disrupted during the early postnatal period. It is possible that as a consequence of the disruption, these motoneurones become susceptible to the excitatory inputs they receive within the maturing central nervous system. In this thesis, the role of afferent activity in the survival of motoneurones after target-deprivation in neonatal rats was examined. In the first part of the thesis, the effect of increasing the level of afferent input to motoneurones during the early postnatal period was investigated. Inducing premature locomotor activity in the neonate resulted in the death of a proportion of otherwise normal motoneurones to the slow, soleus muscle but not of those to the fast, TA and EDL muscles. The effect of increased afferent activity on the survival of motoneurones that had been deprived of target contact was also investigated. Inducing locomotor activity in these rats resulted in a further decrease of motoneurone survival. In the second part of the thesis, the effect of decreasing the level of afferent input to motoneurones that were destined to die after neonatal target-deprivation was studied- Several approaches aimed at decreasing the level of afferent input to motoneurones were used. Decreasing the segmental afferent activity did not affect the survival of these motoneurones. However, reducing the effects of glutamate, the main excitatory neurotransmitter in the spinal cord, by blocking the NMDA receptor with MK-801 resulted in greater survival of the target-deprived motoneurones. The results in this study support the proposal that afferent activity plays an important role in determining the survival of motoneurones deprived of target interaction during a critical period of their development.