Galanin, a 29-amino-acid peptide expressed in dorsal root ganglia (DRG) and spinal dorsal horn interneurones, is regulated by nerve injury and peripheral inflammation. The functional significance of such regulation has been subject to intense studies, including the analysis of galanin null mice, with the production of apparently conflicting results. Here, we suggest that upregulation of galanin in DRG neurones following nerve injury results in antinociception via stimulation of galanin GAL1 receptors on dorsal horn neurones, and that the pro-nociceptive effect of galanin is related to presynaptic galanin GAL2 receptors on primary afferents. A selective GAL1 receptor agonist could therefore be valuable for the treatment of neuropathic pain.