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Letters to Nature
Nature 355, 75 - 78 (02 January 1992); doi:10.1038/355075a0

Peripheral nerve injury triggers central sprouting of myelinated afferents

Clifford J. Woolf, Peter Shortland & Richard E. Coggeshall*

Department of Anatomy and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK
* Department of Anatomy and Neuroscience, University of Texas Medical Branch, University Blvd, Galveston, Texas 77550, USA

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 Abeta 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 humans8,9.

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