Reduced spinal microglial activation and neuropathic pain after nerve injury in mice lacking all three nitric oxide synthases

摘要

BackgroundSeveral studies have investigated the involvement of nitric oxide (NO) in acute and chronic pain using mice lacking a single NO synthase (NOS) gene among the three isoforms: neuronal (nNOS), inducible (iNOS) and endothelial (eNOS). However, the precise role of NOS/NO in pain states remains to be determined owing to the substantial compensatory interactions among the NOS isoforms. Therefore, in this study, we used mice lacking all three NOS genes (n/i/eNOS^-/-mice) and investigated the behavioral phenotypes in a series of acute and chronic pain assays.