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Activity-dependent plasticity in the spinal dorsal horn may underlie the development of neuropathic pain following peripheral nerve injury. A product of an immediate early gene (IEG), the synaptic scaffolding protein Homer1a, has received increasing attention because it appears to play a critical role in synaptic plasticity. In this study, we explored the early expression of Homer1 gene in the spinal dorsal horn by using the neuropathic pain model of chronic compression of dorsal root ganglion (CCD). The levels of Homer1a mRNA in the ipsilateral dorsal horn of CCD rats were markedly increased at 4 hr, remained elevated at 8 hr, and then returned to baseline values by 24 hr after CCD treatment. In contrast, there were no significant changes of Homer1a expression in the Sham-operated or Control groups. Significant thermal hyperalgesia appeared at 24 hr post-operation in the CCD rats, but not in the Shamoperated or Control groups. These data show that CCD induces a transient and rapid increase in Homer1a expression in the spinal dorsal horn. These data also suggest that the transient and rapid increase in Homer1a expression may play an important role in the thermal hyperalgesia elicited by neural injury.