THE central terminals of primary afferent neurons are topographically highly ordered in the spinal cord¹. Peripheral receptor sensitivity is reflected by dorsal horn laminar location: low-threshold mechanoreceptors terminate in laminae III and IV (refs 2, 3) and high-threshold nociceptors in laminae I, II and V (refs 4, 5). Unmyelinated C fibres, most of which are nociceptors⁶, terminate predominantly in lamina II (refs 5,7). There is therefore an anatomical framework for the transfer of specific inputs to localized subsets of dorsal horn neurons. This specificity must contribute to the relationship between a low-intensity stimulus and an innocuous sensation and a noxious stimulus and pain. We now show that after peripheral nerve injury the central terminals of axotomized myelinated afferents, including the large Aβ fibres, sprout into lamina II. This structural reorganization in the adult central nervous system may contribute to the development of the pain mediated by A-fibres that can follow nerve lesions in humans^8,9.