We have known for many years that the spinal cord can generate some basic locomotor outputs under specific experimental conditions without any input from the brain or the periphery (Stuart and Hultborn, 2008). However, when inputs from the brain are lost following spinal cord injury (SCI), the mammalian spinal cord is unable to generate normal, goal-directed locomotor outputs. In contrast, lower vertebrates spontaneously regenerate axons across lesion sites and recover locomotor function after complete spinal cord lesions (Cohen et al., 1988). The major focus of research into SCI in mammals has been to replicate this lower vertebrate capability by promoting the regeneration of lesioned axons or the sprouting of processes from spared axons, with the aim of reconnecting the spinal cord and thus repairing the damage caused by the injury (Steward et al., 2012). It is not that regeneration cannot occur in mammals, but it is instead actively inhibited. Why this inhibition has evolved in mammals is unknown. It would be useful to consider this question as it may help to explain why the various regeneration strategies that can successfully overcome this inhibition have so far failed to translate into an effective treatment for SCI (Steward et al., 2012). This article reviews work that we have done on the functional changes after recovery from SCI in the lamprey (Parker, 2017), and how these changes may relate to functional recovery in mammalian systems