Neural recognition molecules were discovered and characterized initially for their functional roles in cell adhesion as regulators of affinity between cells and the extracellular matrix in vitro. They were then recognized as mediators or co-receptors which trigger signal transduction mechanisms affecting cell adhesion and de-adhesion. Their involvement in contact attraction and repulsion relies on cell-intrinsic properties that are modulated by the spatial contexts of their expression at particular stages of ontogenetic development, in synaptic plasticity and during regeneration after injury. The functional roles of recognition molecules in cell proliferation and migration, determination of developmental fate, growth cone guidance, and synapse formation, stabilization and modulation have been well documented not only by in vitro, but also by in vivo studies that have been greatly aided by generation of genetically altered mice. More recently, the functions of recognition molecules have been investigated under conditions of neural repair and manipulated using a broad range of genetic and pharmacological approaches to achieve a beneficial outcome. The principal aim of most therapeutically oriented approaches has been to neutralize inhibitory factors. However, less attention has been paid to enhancing repair by stimulating the stimulatory factors. When considering potential therapeutic strategies, it is worth considering that a single recognition molecule can possess domains that are conducive or repellent and that the spatial distribution of recognition molecules can determine the overall function: Recognition molecules may be repellent for neurite outgrowth when presented as barriers or steep-concentration gradients and conducive when presented as uniform substrates. The focus of this review will be on the more recent attempts to study the conducive mechanisms with the expectation that they may be able to tip the balance from a regeneration inhospitable to a hospitable environment. It is likely that a combination of the two principles, as multifactorial as each principle may be in itself, will be of therapeutic value in humans. Keywords: astrogliosis, chondroitin sulfate proteoglycans, close homolog of L1, collagen, immunoglobulin superfamily, neural cell adhesion molecule, neurite outgrowth, neuronal cell adhesion molecule L1, neuronal survival, Nogo, regeneration, signal transduction, tenascins, trauma. Like cells in other tissues, cells in the nervous system depend on temporally and spatially precise tuning of interactions with each other and their extracellular matrix environment. Recognition molecules mediate these interactions during ontogenetic development, beginning with neural induction and continuing with cell proliferation and migration, determination of developmental fate, guided neurite outgrowth, and synapse formation, stabilization, and modulation. With age and in neurodegenerative disorders, these interactions succumb to reduced adaptation to the needs of the organism. Recognition molecule...