Many studies have shown that galanin and neuropathic pain has been associated, but lack of galanin and its receptor changes after the median nerve injury and on the median neuropathic pain. In this study, we used the median nerve chronic constriction injury model to serve as the carpal tunnel syndrome, and to investigate the role of galanin and its receptor in the upper limb neuropathic pain. Present results showed that the galanin-immunoreatice like (-IL) neurons were exclusively small-size DRG neurons in the naïve rats. After a week of the median nerve chronic constriction injury, the percentage of galanin-IL neurons and the proportion of them with medium- and large-size both significantly increase. We also used immunofluorescence (IF) double labeling to investigate the relationship between galanin and pain-related factors: vanilloid receptor subtype 1 (TRPV1), P2X3 and growth-associated protein-43 (GAP-43) in the C6 DRG after a week of the median nerve chronic constriction injury. We found that the number and percentage of the above-mentioned double labeling neurons in the injured DRG all have markedly increased. Futhermore, lidocaine treatment prior to median nerve chronic constriction injury, increase in the number of galanin–IL neurons in the DRG was dramatically slow down. This study also showed that one week after injury the number of galanin receptor 2 (GalR2)-IL neurons in the injured side DRG and cuneate nucleus was significantly higher than those in the normal group. Futhermore, combining fluorogold labeling illustrated that in the cuneate nucleus GalR2-IL neurons dreived mostly from cuneothalamic projection neurons after injury. Finally, our results revealed that the level of allodynia and the number of c-Fos neuron in the cuneate nucleus were both alleviated in the GalR2 antagonist treatment group. The present result suggest that the blocking of galanin receptor 2 may be the target of neuropathic pain relief.