Objective        To investigate the role of spinal glucocorticoid receptor (GR) in the generation and development of chronic neuropathic pain.       Methods        Healthy adult SD rats were divided into a sham group

a chronic compressive injury of sciatic nerve (CCI) group

a CCI+saline group and a CCI+RU38486 group. The thermal withdrawal latency (TWL) was measured before operation and at 1

3

7 and 14 d after operation. The L

4-6

lumbar segment of spinal cord of the rats in the CCI group was separated for the determination of GR expression by immunohistochemical assay. For the rats of the CCI+saline group and the CCI+RU38486

group

saline and RU38486 (GR antagonist) were intrathecally administered twice a day for 14 d after CCI operation.       Results        TWL decreased at 1 d after CCI operation

and thermal hyperalgesia persisted until the end of the experiment. The immunohistochemical results showed that the expression of GR significantly increased in the ipsilateral dorsal horn at 7 and 14 d after CCI operation. However

the intrathecal administration of RU38486 could significantly suppress the decrease of TWL after CCI operation.       Conclusion       The activation of GR in spinal dorsal horn can promote the pathogenesis of neuropathic pain

suggesting that blocking GR may be a viable therapeutic strategy for neuropathic pain.