Axons are essential for neuronal communication but they do not regenerate after injury to the adult mammalian brain or spinal cord. Failed regeneration is due in part to the production of a potent axonal growth inhibitor, Nogo, by myelinating cells. The finding of a high affinity axonal receptor for the extracellular domain of Nogo provides the first insight into the basis of Nogo action. Disrupting the interaction of Nogo with the Nogo-66 receptor may facilitate axonal regeneration in vivo. Th