Critically ill paediatric patients are frequently exposed to pain (Chambliss and Anand 1997) and there are reports of prolonged sensory disturbances and altered pain perception lasting well beyond the infant period in children that have undergone early pain and trauma (Porter et al. 1999). The aim of this thesis was to study the mechanisms underlying such effects. Behavioural and electrophysiological techniques were used to assess both the acute and long term effects of early pain, upon spinal sensory pathways, in the rat. Using 'in vivo' electrophysiological recordings of single dorsal horn cells in urethane anaesthetised rats at different postnatal ages, I have demonstrated that cutaneous afferent evoked activity and receptive field properties of dorsal horn cells undergo considerable postnatal development (Chapter 2). Comparisons were made between spinal sensory processing in normal animals and animals which had received acute inflammation of the hindpaw at different postnatal ages. The characteristic changes in both behaviour and in dorsal horn neuron properties that occur following acute peripheral inflammation in the adult were found to be developmentally regulated (Chapter 3). Hindpaw inflammation at birth, while causing acute effects did not result in any long term behavioural or electrophysiological changes in sensory processing, tested three weeks later. However if the skin was physically wounded in the neonatal period, the receptive field size of sensory dorsal horn cells remained substantially altered three and six weeks later (Chapter 4). This long term alteration in the sensory connections of dorsal horn neurons may provide a physiological mechanism for the prolonged behavioural hypersensitivity that follows early skin wounding (Reynolds and Fitzgerald 1995; De Lima et al. 1999). These results may be relevant to critically ill paediatric patients exposed to pain.