Injury to the mature central nervous system (CNS) induces a series of transient changes leading not only to death of neurons, but also to spontaneous rearrangement of the affected network. One of such pro plastic events, detected following injury, is an increased level of neurotrophins. Neurotrophins are a family of proteins involved in survival and outgrowth processes. The other one, more difficult to observe, is a change in the complexity of the dendritic tree, causing arborization or pruning, depending on many circumstances: i.e. lesion etiology. Subsequent therapies like enriched environment or locomotor exercise bring about a functional improvement, which was found to further increase the neurotrophin level and induced additional arborization of dendrites. Another important consequence of damage to CNS connections is deafferentation, shown to induce a down regulation of outgrowth inhibitors. Their suppression in turn may facilitate dendritic plasticity. Taken together, these factors may contribute to enhanced plasticity in the injured mature CNS. Thus the proper use of endogenously increased plastic potential seems to be important for design and optimizing therapeutic strategies. Further investigation of mechanisms involved in switching on plasticity may help to improve on existing therapies and find new ways to obtain better recovery following injury.