Background and Objectives: To date, there has been no study on the effects of FTY720 on chronic stage of complex regional pain syndrome (CRPS) rodent models, despite the anti-allodynic effect of FTY720 in previous studies. Thus, the aim of this study was to investigate the effect of FTY720 in a CRPS mouse model. 
Method: The authors used a mouse model of CRPS (n = 6/group), involving tibia fracture/cast immobilization, to test the efficacy of intrathecal FTY720 (2μ/kg, 5 μL−1 day−1; 6 days) or vehicle during the chronic (seven weeks after fracture) stage of CRPS. 
Results: Intrathecal recombinant FTY720 administration was anti-allodynic in the chronic stage of the CRPS mouse model, and such effect of FTY720 developed by modulating astrocyte activation in the spinal cord. Additionally, according to the in vitro data, the FTY720 treatment inhibited Sphingosine 1-phosphate induced increase in the nitric oxide production and suppression of the NF-κB pathway, by inhibiting the phosphorylation of NF-κB/p65 in astrocytes without toxic effect on astrocytes. 
Conclusion: Collectively, these results demonstrate that intrathecally administered FTY720 attenuates mechanical allodynia in the chronic stage of CRPS mouse model.

10 - S1PR antagonist Attenuates mechanical allodynia in a mouse model of chronic CRPS by Inhibiting Spinal Reactive Astrocyte-Mediated Neuroinflammation Through the NF-&#954;B Pathway.

10 - S1PR antagonist Attenuates mechanical allodynia in a mouse model of chronic CRPS by Inhibiting Spinal Reactive Astrocyte-Mediated Neuroinflammation Through the NF-&#954;B Pathway.

10 - S1PR antagonist Attenuates mechanical allodynia in a mouse model of chronic CRPS by Inhibiting Spinal Reactive Astrocyte-Mediated Neuroinflammation Through the NF-κB Pathway.