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Neuropathic pain is characterized by a heightened painful response to noxious (hyperalgesia) or innocuous (allodynia) stimulation, and pain at rest (spontaneous pain).At present no effective drug is available for the clinical symptom.A recent study has shown that the translocator protein (TSPO, 18 kDa), a peripheral receptor for benzodiazepine, modulates pain behaviors of rats induced by CFA.In the present study, we evaluated the role of TSPO in neuropthic pain produced by L5 spinal nerve ligation (L5 SNL) with use of behavioral testing, immunohistochemistry and Western blot methods.We found that TSPO was up-regulated in spinal dorsal horn following L5 SNL and the change lasted until behavioral signs of neuropathic pain diminished (around 50 d).Double immunofluorescence showed that in naive rats, TSPO was located mainly in astrocytes, to a lesser extent in neurons, but not in microglia, whereas following L5 SNL, TSPO was upregutated in astrocytes and microglia, but not in neurons.Behavioral data showed that single intrathecal injection of TSPO agonist Ro5-4864 or FGIN-1-27 reversed established mechanical allodynia induced by L5 SNL completely.Immunofluorescence and Western blot showed that intrathecal injection of Ro5-4864 reversed activation of astrocytes, and depressed p38 MAPK activation, which is exclusively activated in spinal microglial cells following peripheral nerve injury.The data suggested that activation of TSPO by agonists might reverse neuropathic pain by inhibition of activated glial cells.