Pain perception is modulated by a complex network of neuronal circuits that ultimately influence nociceptive transmission at the spinal cord. Although a lot of emphasis has been given to the pain inhibitory components, the occurrence of pain facilitation gained increasing relevance during the last years. Its weight on defining ascending nociceptive signalling is, however, far from understood. The role of descending facilitation in pain control was first committed to anti-analgesic actions and the establishment of sensitisation during chronic pain (Lima and Almeida, 2002). The possibility that facilitation is important to tune pain perception and reactions in everyday physiological conditions was brought into consideration after the discover of supraspinal centres that primarily induce increased nocifensive behaviour and enhanced responsiveness of nociceptive neurons. This is the case of the medullary dorsal reticular nucleus (DRt) (Lima and Almeida, 2002) . The DRt was shown to establish closed reciprocal loops with the spinal cord lamina I, as were some inhibitory centres such as the caudal ventrolateral reticular formation (VLM) and the nucleus tractus solitarii (NTS). In lamina I, but not in the deep dorsal horn, axons projecting down from the DRt or the VLM establish synaptic contacts with neurons that in turn synapse upon DRt and VLM lamina I-projecting neurons. While in the first case synapses are excitatory at both spinal and medullary levels (Almeida et al., 1993, 2000), in the latter the spinal link is either excitatory or inhibitory, the inhibitory circuit being dominant (Tavares and Lima, 2002). These reciprocal circuits are well fitted to subserve a direct control of activation of projection neurons from the respective target, and may explain the observed differences in the relative amount of projecting lamina I neurons that are activated in different pathways. Not so easy to explain is the fact that, for the same pathway, different lamina I cell groups are activated in different amounts. Nevertheless, the data imply that for fixed stimulation conditions there is a pattern of supraspinal distribution of nociceptive input determined by the amount of lamina I neurons of different types that contribute to different pathways (Lima, 1998). The activation pattern varies by varying stimulus properties, such as the nature of the stimulus, and desappears in conditions in which discrimination is impaired, such as secondary hyperalgesia. These findings indicate that the structural diversity of lamina I neurons may contribute to adapt ascending nociceptive signalling to stimulation conditions through the differential activation of the various cell groups contributing to the various pathways.